The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.
Regulatory signaling systems that control the progression through the CELL CYCLE. They ensure that the cell has completed, in the correct order and without mistakes, all the processes required to replicate the GENOME and CYTOPLASM, and divide them equally between two daughter cells. If cells sense they have not completed these processes or that the environment does not have the nutrients and growth hormones in place to proceed, then the cells are restrained (or "arrested") until the processes are completed and growth conditions are suitable.
The period of the CELL CYCLE preceding DNA REPLICATION in S PHASE. Subphases of G1 include "competence" (to respond to growth factors), G1a (entry into G1), G1b (progression), and G1c (assembly). Progression through the G1 subphases is effected by limiting growth factors, nutrients, or inhibitors.
Phase of the CELL CYCLE following G1 and preceding G2 when the entire DNA content of the nucleus is replicated. It is achieved by bidirectional replication at multiple sites along each chromosome.
A type of CELL NUCLEUS division by means of which the two daughter nuclei normally receive identical complements of the number of CHROMOSOMES of the somatic cells of the species.
A large family of regulatory proteins that function as accessory subunits to a variety of CYCLIN-DEPENDENT KINASES. They generally function as ENZYME ACTIVATORS that drive the CELL CYCLE through transitions between phases. A subset of cyclins may also function as transcriptional regulators.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
The period from onset of one menstrual bleeding (MENSTRUATION) to the next in an ovulating woman or female primate. The menstrual cycle is regulated by endocrine interactions of the HYPOTHALAMUS; the PITUITARY GLAND; the ovaries; and the genital tract. The menstrual cycle is divided by OVULATION into two phases. Based on the endocrine status of the OVARY, there is a FOLLICULAR PHASE and a LUTEAL PHASE. Based on the response in the ENDOMETRIUM, the menstrual cycle is divided into a proliferative and a secretory phase.
The period of the CELL CYCLE following DNA synthesis (S PHASE) and preceding M PHASE (cell division phase). The CHROMOSOMES are tetraploid in this point.
A cyclin-dependent kinase inhibitor that mediates TUMOR SUPPRESSOR PROTEIN P53-dependent CELL CYCLE arrest. p21 interacts with a range of CYCLIN-DEPENDENT KINASES and associates with PROLIFERATING CELL NUCLEAR ANTIGEN and CASPASE 3.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A cyclin-dependent kinase inhibitor that coordinates the activation of CYCLIN and CYCLIN-DEPENDENT KINASES during the CELL CYCLE. It interacts with active CYCLIN D complexed to CYCLIN-DEPENDENT KINASE 4 in proliferating cells, while in arrested cells it binds and inhibits CYCLIN E complexed to CYCLIN-DEPENDENT KINASE 2.
Product of the retinoblastoma tumor suppressor gene. It is a nuclear phosphoprotein hypothesized to normally act as an inhibitor of cell proliferation. Rb protein is absent in retinoblastoma cell lines. It also has been shown to form complexes with the adenovirus E1A protein, the SV40 T antigen, and the human papilloma virus E7 protein.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
CELL CYCLE regulatory signaling systems that are triggered by DNA DAMAGE or lack of nutrients during G2 PHASE. When triggered they restrain cells transitioning from G2 phase to M PHASE.
A quiescent state of cells during G1 PHASE.
Phosphoprotein with protein kinase activity that functions in the G2/M phase transition of the CELL CYCLE. It is the catalytic subunit of the MATURATION-PROMOTING FACTOR and complexes with both CYCLIN A and CYCLIN B in mammalian cells. The maximal activity of cyclin-dependent kinase 1 is achieved when it is fully dephosphorylated.
A cell line derived from cultured tumor cells.
Regulatory signaling systems that control the progression of the CELL CYCLE through the G1 PHASE and allow transition to S PHASE when the cells are ready to undergo DNA REPLICATION. DNA DAMAGE, or the deficiencies in specific cellular components or nutrients may cause the cells to halt before progressing through G1 phase.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
A key regulator of CELL CYCLE progression. It partners with CYCLIN E to regulate entry into S PHASE and also interacts with CYCLIN A to phosphorylate RETINOBLASTOMA PROTEIN. Its activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P27 and CYCLIN-DEPENDENT KINASE INHIBITOR P21.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
Protein encoded by the bcl-1 gene which plays a critical role in regulating the cell cycle. Overexpression of cyclin D1 is the result of bcl-1 rearrangement, a t(11;14) translocation, and is implicated in various neoplasms.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
The process by which a DNA molecule is duplicated.
A 50-kDa protein that complexes with CYCLIN-DEPENDENT KINASE 2 in the late G1 phase of the cell cycle.
Genes that code for proteins that regulate the CELL DIVISION CYCLE. These genes form a regulatory network that culminates in the onset of MITOSIS by activating the p34cdc2 protein (PROTEIN P34CDC2).
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
Established cell cultures that have the potential to propagate indefinitely.
A cyclin subtype that has specificity for CDC2 PROTEIN KINASE and CYCLIN-DEPENDENT KINASE 2. It plays a role in progression of the CELL CYCLE through G1/S and G2/M phase transitions.
The interval between two successive CELL DIVISIONS during which the CHROMOSOMES are not individually distinguishable. It is composed of the G phases (G1 PHASE; G0 PHASE; G2 PHASE) and S PHASE (when DNA replication occurs).
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
A cyclin subtype that is transported into the CELL NUCLEUS at the end of the G2 PHASE. It stimulates the G2/M phase transition by activating CDC2 PROTEIN KINASE.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
Cyclin-dependent kinase 4 is a key regulator of G1 PHASE of the CELL CYCLE. It partners with CYCLIN D to phosphorylate RETINOBLASTOMA PROTEIN. CDK4 activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P16.
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
Proteins that are normally involved in holding cellular growth in check. Deficiencies or abnormalities in these proteins may lead to unregulated cell growth and tumor development.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
A family of cell cycle-dependent kinases that are related in structure to CDC28 PROTEIN KINASE; S CEREVISIAE; and the CDC2 PROTEIN KINASE found in mammalian species.
The period of cyclic physiological and behavior changes in non-primate female mammals that exhibit ESTRUS. The estrous cycle generally consists of 4 or 5 distinct periods corresponding to the endocrine status (PROESTRUS; ESTRUS; METESTRUS; DIESTRUS; and ANESTRUS).
A subclass of dual specificity phosphatases that play a role in the progression of the CELL CYCLE. They dephosphorylate and activate CYCLIN-DEPENDENT KINASES.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
A family of basic helix-loop-helix transcription factors that control expression of a variety of GENES involved in CELL CYCLE regulation. E2F transcription factors typically form heterodimeric complexes with TRANSCRIPTION FACTOR DP1 or transcription factor DP2, and they have N-terminal DNA binding and dimerization domains. E2F transcription factors can act as mediators of transcriptional repression or transcriptional activation.
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.
Elements of limited time intervals, contributing to particular results or situations.
A cyclin B subtype that colocalizes with MICROTUBULES during INTERPHASE and is transported into the CELL NUCLEUS at the end of the G2 PHASE.
A species of the genus SACCHAROMYCES, family Saccharomycetaceae, order Saccharomycetales, known as "baker's" or "brewer's" yeast. The dried form is used as a dietary supplement.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
A cyclin subtype that is specific for CYCLIN-DEPENDENT KINASE 4 and CYCLIN-DEPENDENT KINASE 6. Unlike most cyclins, cyclin D expression is not cyclical, but rather it is expressed in response to proliferative signals. Cyclin D may therefore play a role in cellular responses to mitogenic signals.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
A series of oxidative reactions in the breakdown of acetyl units derived from GLUCOSE; FATTY ACIDS; or AMINO ACIDS by means of tricarboxylic acid intermediates. The end products are CARBON DIOXIDE, water, and energy in the form of phosphate bonds.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
A nucleoside that substitutes for thymidine in DNA and thus acts as an antimetabolite. It causes breaks in chromosomes and has been proposed as an antiviral and antineoplastic agent. It has been given orphan drug status for use in the treatment of primary brain tumors.
An E2F transcription factor that interacts directly with RETINOBLASTOMA PROTEIN and CYCLIN A and activates GENETIC TRANSCRIPTION required for CELL CYCLE entry and DNA synthesis. E2F1 is involved in DNA REPAIR and APOPTOSIS.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Proteins obtained from the species SACCHAROMYCES CEREVISIAE. The function of specific proteins from this organism are the subject of intense scientific interest and have been used to derive basic understanding of the functioning similar proteins in higher eukaryotes.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Cell regulatory signaling system that controls progression through S PHASE and stabilizes the replication forks during conditions that could affect the fidelity of DNA REPLICATION, such as DNA DAMAGE or depletion of nucleotide pools.
A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
A broadly expressed type D cyclin. Experiments using KNOCKOUT MICE suggest a role for cyclin D3 in LYMPHOCYTE development.
A group of cell cycle proteins that negatively regulate the activity of CYCLIN/CYCLIN-DEPENDENT KINASE complexes. They inhibit CELL CYCLE progression and help control CELL PROLIFERATION following GENOTOXIC STRESS as well as during CELL DIFFERENTIATION.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Proteins found in any species of fungus.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
A genus of ascomycetous fungi of the family Schizosaccharomycetaceae, order Schizosaccharomycetales.
Small chromosomal proteins (approx 12-20 kD) possessing an open, unfolded structure and attached to the DNA in cell nuclei by ionic linkages. Classification into the various types (designated histone I, histone II, etc.) is based on the relative amounts of arginine and lysine in each.
The cellular signaling system that halts the progression of cells through MITOSIS or MEIOSIS if a defect that will affect CHROMOSOME SEGREGATION is detected.
Nuclear antigen with a role in DNA synthesis, DNA repair, and cell cycle progression. PCNA is required for the coordinated synthesis of both leading and lagging strands at the replication fork during DNA replication. PCNA expression correlates with the proliferation activity of several malignant and non-malignant cell types.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
High molecular weight proteins found in the MICROTUBULES of the cytoskeletal system. Under certain conditions they are required for TUBULIN assembly into the microtubules and stabilize the assembled microtubules.
Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
An antineoplastic agent that inhibits DNA synthesis through the inhibition of ribonucleoside diphosphate reductase.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
A product of the p16 tumor suppressor gene (GENES, P16). It is also called INK4 or INK4A because it is the prototype member of the INK4 CYCLIN-DEPENDENT KINASE INHIBITORS. This protein is produced from the alpha mRNA transcript of the p16 gene. The other gene product, produced from the alternatively spliced beta transcript, is TUMOR SUPPRESSOR PROTEIN P14ARF. Both p16 gene products have tumor suppressor functions.
A species of gram-negative, aerobic bacteria that consist of slender vibroid cells.
Cyclin-dependent kinase 6 associates with CYCLIN D and phosphorylates RETINOBLASTOMA PROTEIN during G1 PHASE of the CELL CYCLE. It helps regulate the transition to S PHASE and its kinase activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P18.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
A cyclin D subtype which is regulated by GATA4 TRANSCRIPTION FACTOR. Experiments using KNOCKOUT MICE suggest a role for cyclin D2 in granulosa cell proliferation and gonadal development.
A transcription factor that possesses DNA-binding and E2F-binding domains but lacks a transcriptional activation domain. It is a binding partner for E2F TRANSCRIPTION FACTORS and enhances the DNA binding and transactivation function of the DP-E2F complex.
3-Hydroxy-4-oxo-1(4H)-pyridinealanine. An antineoplastic alanine-substituted pyridine derivative isolated from Leucena glauca.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Complexes of enzymes that catalyze the covalent attachment of UBIQUITIN to other proteins by forming a peptide bond between the C-terminal GLYCINE of UBIQUITIN and the alpha-amino groups of LYSINE residues in the protein. The complexes play an important role in mediating the selective-degradation of short-lived and abnormal proteins. The complex of enzymes can be broken down into three components that involve activation of ubiquitin (UBIQUITIN-ACTIVATING ENZYMES), conjugation of ubiquitin to the ligase complex (UBIQUITIN-CONJUGATING ENZYMES), and ligation of ubiquitin to the substrate protein (UBIQUITIN-PROTEIN LIGASES).
Transport proteins that carry specific substances in the blood or across cell membranes.
A gene silencing phenomenon whereby specific dsRNAs (RNA, DOUBLE-STRANDED) trigger the degradation of homologous mRNA (RNA, MESSENGER). The specific dsRNAs are processed into SMALL INTERFERING RNA (siRNA) which serves as a guide for cleavage of the homologous mRNA in the RNA-INDUCED SILENCING COMPLEX. DNA METHYLATION may also be triggered during this process.
The rate dynamics in chemical or physical systems.
A ubiquitously expressed regulatory protein that contains a retinoblastoma protein binding domain and an AT-rich interactive domain. The protein may play a role in recruiting HISTONE DEACETYLASES to the site of RETINOBLASTOMA PROTEIN-containing transcriptional repressor complexes.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
A microtubule structure that forms during CELL DIVISION. It consists of two SPINDLE POLES, and sets of MICROTUBULES that may include the astral microtubules, the polar microtubules, and the kinetochore microtubules.
The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.
The continuous sequence of changes undergone by living organisms during the post-embryonic developmental process, such as metamorphosis in insects and amphibians. This includes the developmental stages of apicomplexans such as the malarial parasite, PLASMODIUM FALCIPARUM.
An E3 ubiquitin ligase primarily involved in regulation of the metaphase-to-anaphase transition during MITOSIS through ubiquitination of specific CELL CYCLE PROTEINS. Enzyme activity is tightly regulated through subunits and cofactors, which modulate activation, inhibition, and substrate specificity. The anaphase-promoting complex, or APC-C, is also involved in tissue differentiation in the PLACENTA, CRYSTALLINE LENS, and SKELETAL MUSCLE, and in regulation of postmitotic NEURONAL PLASTICITY and excitability.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
Hybridization of a nucleic acid sample to a very large set of OLIGONUCLEOTIDE PROBES, which have been attached individually in columns and rows to a solid support, to determine a BASE SEQUENCE, or to detect variations in a gene sequence, GENE EXPRESSION, or for GENE MAPPING.
Proteins obtained from the species Schizosaccharomyces pombe. The function of specific proteins from this organism are the subject of intense scientific interest and have been used to derive basic understanding of the functioning similar proteins in higher eukaryotes.
The cell center, consisting of a pair of CENTRIOLES surrounded by a cloud of amorphous material called the pericentriolar region. During interphase, the centrosome nucleates microtubule outgrowth. The centrosome duplicates and, during mitosis, separates to form the two poles of the mitotic spindle (MITOTIC SPINDLE APPARATUS).
Cellular DNA-binding proteins encoded by the c-myc genes. They are normally involved in nucleic acid metabolism and in mediating the cellular response to growth factors. Elevated and deregulated (constitutive) expression of c-myc proteins can cause tumorigenesis.
Nocodazole is an antineoplastic agent which exerts its effect by depolymerizing microtubules.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Cell lines whose original growing procedure consisted being transferred (T) every 3 days and plated at 300,000 cells per plate (J Cell Biol 17:299-313, 1963). Lines have been developed using several different strains of mice. Tissues are usually fibroblasts derived from mouse embryos but other types and sources have been developed as well. The 3T3 lines are valuable in vitro host systems for oncogenic virus transformation studies, since 3T3 cells possess a high sensitivity to CONTACT INHIBITION.
A widely-expressed cyclin A subtype that functions during the G1/S and G2/M transitions of the CELL CYCLE.
Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye.
A protein kinase encoded by the Saccharomyces cerevisiae CDC28 gene and required for progression from the G1 PHASE to the S PHASE in the CELL CYCLE.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Proteins which maintain the transcriptional quiescence of specific GENES or OPERONS. Classical repressor proteins are DNA-binding proteins that are normally bound to the OPERATOR REGION of an operon, or the ENHANCER SEQUENCES of a gene until a signal occurs that causes their release.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in fungi.
A group of PROTEIN-SERINE-THREONINE KINASES which activate critical signaling cascades in double strand breaks, APOPTOSIS, and GENOTOXIC STRESS such as ionizing ultraviolet A light, thereby acting as a DNA damage sensor. These proteins play a role in a wide range of signaling mechanisms in cell cycle control.
Enzyme activated in response to DNA DAMAGE involved in cell cycle arrest. The gene is located on the long (q) arm of chromosome 22 at position 12.1. In humans it is encoded by the CHEK2 gene.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action during the developmental stages of an organism.
A genus of gram-negative, aerobic, rod- or vibroid-shaped or fusiform bacteria that commonly produce a stalk. They are found in fresh water and soil and divide by binary transverse fission.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
The functional hereditary units of FUNGI.
The material of CHROMOSOMES. It is a complex of DNA; HISTONES; and nonhistone proteins (CHROMOSOMAL PROTEINS, NON-HISTONE) found within the nucleus of a cell.
A family of structurally-related proteins that were originally identified by their ability to complex with cyclin proteins (CYCLINS). They share a common domain that binds specifically to F-BOX MOTIFS. They take part in SKP CULLIN F-BOX PROTEIN LIGASES, where they can bind to a variety of F-BOX PROTEINS.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
The decrease in the cell's ability to proliferate with the passing of time. Each cell is programmed for a certain number of cell divisions and at the end of that time proliferation halts. The cell enters a quiescent state after which it experiences CELL DEATH via the process of APOPTOSIS.
Penetrating, high-energy electromagnetic radiation emitted from atomic nuclei during NUCLEAR DECAY. The range of wavelengths of emitted radiation is between 0.1 - 100 pm which overlaps the shorter, more energetic hard X-RAYS wavelengths. The distinction between gamma rays and X-rays is based on their radiation source.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
Proteins whose abnormal expression (gain or loss) are associated with the development, growth, or progression of NEOPLASMS. Some neoplasm proteins are tumor antigens (ANTIGENS, NEOPLASM), i.e. they induce an immune reaction to their tumor. Many neoplasm proteins have been characterized and are used as tumor markers (BIOMARKERS, TUMOR) when they are detectable in cells and body fluids as monitors for the presence or growth of tumors. Abnormal expression of ONCOGENE PROTEINS is involved in neoplastic transformation, whereas the loss of expression of TUMOR SUPPRESSOR PROTEINS is involved with the loss of growth control and progression of the neoplasm.
An antiviral antibiotic produced by Cephalosporium aphidicola and other fungi. It inhibits the growth of eukaryotic cells and certain animal viruses by selectively inhibiting the cellular replication of DNA polymerase II or the viral-induced DNA polymerases. The drug may be useful for controlling excessive cell proliferation in patients with cancer, psoriasis or other dermatitis with little or no adverse effect upon non-multiplying cells.
Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.
A potent inhibitor of CYCLIN-DEPENDENT KINASES in G1 PHASE and S PHASE. In humans, aberrant expression of p57 is associated with various NEOPLASMS as well as with BECKWITH-WIEDEMANN SYNDROME.
Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein TUBULIN and are influenced by TUBULIN MODULATORS.
The part of a cell that contains the CYTOSOL and small structures excluding the CELL NUCLEUS; MITOCHONDRIA; and large VACUOLES. (Glick, Glossary of Biochemistry and Molecular Biology, 1990)
A negative regulator of the CELL CYCLE that undergoes PHOSPHORYLATION by CYCLIN-DEPENDENT KINASES. It contains a conserved pocket region that binds E2F4 TRANSCRIPTION FACTOR and interacts with viral ONCOPROTEINS such as POLYOMAVIRUS TUMOR ANTIGENS; ADENOVIRUS E1A PROTEINS; and PAPILLOMAVIRUS E7 PROTEINS.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
Tumors or cancer of the human BREAST.
Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.
A type of CELL NUCLEUS division, occurring during maturation of the GERM CELLS. Two successive cell nucleus divisions following a single chromosome duplication (S PHASE) result in daughter cells with half the number of CHROMOSOMES as the parent cells.
Proteins and peptides that are involved in SIGNAL TRANSDUCTION within the cell. Included here are peptides and proteins that regulate the activity of TRANSCRIPTION FACTORS and cellular processes in response to signals from CELL SURFACE RECEPTORS. Intracellular signaling peptide and proteins may be part of an enzymatic signaling cascade or act through binding to and modifying the action of other signaling factors.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
A cyclin subtype that is found associated with CYCLIN-DEPENDENT KINASE 5; cyclin G associated kinase, and PROTEIN PHOSPHATASE 2.
Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Endogenous or exogenous substances which inhibit the normal growth of human and animal cells or micro-organisms, as distinguished from those affecting plant growth (= PLANT GROWTH REGULATORS).
Tumor suppressor genes located on the short arm of human chromosome 17 and coding for the phosphoprotein p53.
That portion of the electromagnetic spectrum immediately below the visible range and extending into the x-ray frequencies. The longer wavelengths (near-UV or biotic or vital rays) are necessary for the endogenous synthesis of vitamin D and are also called antirachitic rays; the shorter, ionizing wavelengths (far-UV or abiotic or extravital rays) are viricidal, bactericidal, mutagenic, and carcinogenic and are used as disinfectants.
The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.
A large multisubunit complex that plays an important role in the degradation of most of the cytosolic and nuclear proteins in eukaryotic cells. It contains a 700-kDa catalytic sub-complex and two 700-kDa regulatory sub-complexes. The complex digests ubiquitinated proteins and protein activated via ornithine decarboxylase antizyme.
A microtubule subunit protein found in large quantities in mammalian brain. It has also been isolated from SPERM FLAGELLUM; CILIA; and other sources. Structurally, the protein is a dimer with a molecular weight of approximately 120,000 and a sedimentation coefficient of 5.8S. It binds to COLCHICINE; VINCRISTINE; and VINBLASTINE.
A furanyl adenine found in PLANTS and FUNGI. It has plant growth regulation effects.
Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
Proteins prepared by recombinant DNA technology.
Eukaryotic cell line obtained in a quiescent or stationary phase which undergoes conversion to a state of unregulated growth in culture, resembling an in vitro tumor. It occurs spontaneously or through interaction with viruses, oncogenes, radiation, or drugs/chemicals.
Processes that stimulate the GENETIC TRANSCRIPTION of a gene or set of genes.
A diverse class of enzymes that interact with UBIQUITIN-CONJUGATING ENZYMES and ubiquitination-specific protein substrates. Each member of this enzyme group has its own distinct specificity for a substrate and ubiquitin-conjugating enzyme. Ubiquitin-protein ligases exist as both monomeric proteins multiprotein complexes.
A genetic rearrangement through loss of segments of DNA or RNA, bringing sequences which are normally separated into close proximity. This deletion may be detected using cytogenetic techniques and can also be inferred from the phenotype, indicating a deletion at one specific locus.
The artificial induction of GENE SILENCING by the use of RNA INTERFERENCE to reduce the expression of a specific gene. It includes the use of DOUBLE-STRANDED RNA, such as SMALL INTERFERING RNA and RNA containing HAIRPIN LOOP SEQUENCE, and ANTI-SENSE OLIGONUCLEOTIDES.
An E3 UBIQUITIN LIGASE that interacts with and inhibits TUMOR SUPPRESSOR PROTEIN P53. Its ability to ubiquitinate p53 is regulated by TUMOR SUPPRESSOR PROTEIN P14ARF.
Deoxyribonucleic acid that makes up the genetic material of fungi.
An E2F transcription factor that interacts directly with RETINOBLASTOMA PROTEIN and CYCLIN A. E2F2 activates GENETIC TRANSCRIPTION required for CELL CYCLE entry and DNA synthesis.
The developmental entity of a fertilized egg (ZYGOTE) in animal species other than MAMMALS. For chickens, use CHICK EMBRYO.
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
Female germ cells derived from OOGONIA and termed OOCYTES when they enter MEIOSIS. The primary oocytes begin meiosis but are arrested at the diplotene state until OVULATION at PUBERTY to give rise to haploid secondary oocytes or ova (OVUM).
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
The entity of a developing mammal (MAMMALS), generally from the cleavage of a ZYGOTE to the end of embryonic differentiation of basic structures. For the human embryo, this represents the first two months of intrauterine development preceding the stages of the FETUS.
The quantity of volume or surface area of CELLS.
Compounds that inhibit cell production of DNA or RNA.
Proteins that originate from insect species belonging to the genus DROSOPHILA. The proteins from the most intensely studied species of Drosophila, DROSOPHILA MELANOGASTER, are the subject of much interest in the area of MORPHOGENESIS and development.
Proteins coded by oncogenes. They include proteins resulting from the fusion of an oncogene and another gene (ONCOGENE PROTEINS, FUSION).
An expression of the number of mitoses found in a stated number of cells.
Nucleoproteins, which in contrast to HISTONES, are acid insoluble. They are involved in chromosomal functions; e.g. they bind selectively to DNA, stimulate transcription resulting in tissue-specific RNA synthesis and undergo specific changes in response to various hormones or phytomitogens.
Geminin inhibits DNA replication by preventing the incorporation of MCM complex into pre-replication complex. It is absent during G1 phase of the CELL CYCLE and accumulates through S, G2,and M phases. It is degraded at the metaphase-anaphase transition by the ANAPHASE-PROMOTING COMPLEX-CYCLOSOME.
Interruption or suppression of the expression of a gene at transcriptional or translational levels.
A CELL CYCLE and tumor growth marker which can be readily detected using IMMUNOCYTOCHEMISTRY methods. Ki-67 is a nuclear antigen present only in the nuclei of cycling cells.
The phase of cell nucleus division following PROMETAPHASE, in which the CHROMOSOMES line up across the equatorial plane of the SPINDLE APPARATUS prior to separation.
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.
A cyclin A subtype primarily found in male GERM CELLS. It may play a role in the passage of SPERMATOCYTES into meiosis I.
The property of objects that determines the direction of heat flow when they are placed in direct thermal contact. The temperature is the energy of microscopic motions (vibrational and translational) of the particles of atoms.
DNA present in neoplastic tissue.
Trans-acting proteins which accelerate retroviral virus replication. The vpr proteins act in trans to increase the levels of specified proteins. vpr is short for viral protein R, where R is undefined.
A cyclin G subtype that is constitutively expressed throughout the cell cycle. Cyclin G1 is considered a major transcriptional target of TUMOR SUPPRESSOR PROTEIN P53 and is highly induced in response to DNA damage.
A promyelocytic cell line derived from a patient with ACUTE PROMYELOCYTIC LEUKEMIA. HL-60 cells lack specific markers for LYMPHOID CELLS but express surface receptors for FC FRAGMENTS and COMPLEMENT SYSTEM PROTEINS. They also exhibit phagocytic activity and responsiveness to chemotactic stimuli. (From Hay et al., American Type Culture Collection, 7th ed, pp127-8)
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.

Drosophila oogenesis: versatile spn doctors. (1/24243)

Recent work on Drosophila oogenesis has uncovered connections between cell-cycle checkpoints and pattern formation. Genes of the spindle class, which encode double-strand break repair enzymes and RNA helicases, affect oocyte polarity and the decision whether to differentiate as an oocyte or a nurse cell.  (+info)

Transformation mediated by RhoA requires activity of ROCK kinases. (2/24243)

BACKGROUND: The Ras-related GTPase RhoA controls signalling processes required for cytoskeletal reorganisation, transcriptional regulation, and transformation. The ability of RhoA mutants to transform cells correlates not with transcription but with their ability to bind ROCK-I, an effector kinase involved in cytoskeletal reorganisation. We used a recently developed specific ROCK inhibitor, Y-27632, and ROCK truncation mutants to investigate the role of ROCK kinases in transcriptional activation and transformation. RESULTS: In NIH3T3 cells, Y-27632 did not prevent the activation of serum response factor, transcription of c-fos or cell cycle re-entry following serum stimulation. Repeated treatment of NIH3T3 cells with Y-27632, however, substantially disrupted their actin fibre network but did not affect their growth rate. Y-27632 blocked focus formation by RhoA and its guanine-nucleotide exchange factors Dbl and mNET1. It did not affect the growth rate of cells transformed by Dbl and mNET1, but restored normal growth control at confluence and prevented their growth in soft agar. Y-27632 also significantly inhibited focus formation by Ras, but had no effect on the establishment or maintenance of transformation by Src. Furthermore, it significantly inhibited anchorage-independent growth of two out of four colorectal tumour cell lines. Consistent with these data, a truncated ROCK derivative exhibited weak ability to cooperate with activated Raf in focus formation assays. CONCLUSIONS: ROCK signalling is required for both the establishment and maintenance of transformation by constitutive activation of RhoA, and contributes to the Ras-transformed phenotype. These observations provide a potential explanation for the requirement for Rho in Ras-mediated transformation. Moreover, the inhibition of ROCK kinases may be of therapeutic use.  (+info)

Difference between mammary epithelial cells from mature virgin and primiparous mice. (3/24243)

Mammary epithelial cells from mature virgin mice are similar to those from primiparous mice in several respects. However, there is one known difference. The cells from the mature virgin must traverse the cell cycle in order to become competent to make casein and enzymatically active alpha-lactalbumin in vitro; those from the primiparous animal can make these proteins without first traversing the cycle. In this regard, cells from human placental lactogen- and prolactin-treated mature virgins are, after involution, similar to those from primiparous mice. The developemental block in the cells from the mature virgin, imposed by preventing cell cycle traversal, has been partially delineated. It does not appear to reside at the levels of ultrastructural maturation or the formation of casein messenger RNA. Rather, the lesion is postranscriptional and may be at the level of translation, or posttranslational modification, or both.  (+info)

The role of RBF in the introduction of G1 regulation during Drosophila embryogenesis. (4/24243)

The first appearance of G1 during Drosophila embryogenesis, at cell cycle 17, is accompanied by the down-regulation of E2F-dependent transcription. Mutant alleles of rbf were generated and analyzed to determine the role of RBF in this process. Embryos lacking both maternal and zygotic RBF products show constitutive expression of PCNA and RNR2, two E2F-regulated genes, indicating that RBF is required for their transcriptional repression. Despite the ubiquitous expression of E2F target genes, most epidermal cells enter G1 normally. Rather than pausing in G1 until the appropriate time for cell cycle progression, many of these cells enter an ectopic S-phase. These results indicate that the repression of E2F target genes by RBF is necessary for the maintenance but not the initiation of a G1 phase. The phenotype of RBF-deficient embryos suggests that rbf has a function that is complementary to the roles of dacapo and fizzy-related in the introduction of G1 during Drosophila embryogenesis.  (+info)

Coupling of the cell cycle and myogenesis through the cyclin D1-dependent interaction of MyoD with cdk4. (5/24243)

Proliferating myoblasts express the muscle determination factor, MyoD, throughout the cell cycle in the absence of differentiation. Here we show that a mitogen-sensitive mechanism, involving the direct interaction between MyoD and cdk4, restricts myoblast differentiation to cells that have entered into the G0 phase of the cell cycle under mitogen withdrawal. Interaction between MyoD and cdk4 disrupts MyoD DNA-binding, muscle-specific gene activation and myogenic conversion of 10T1/2 cells independently of cyclin D1 and the CAK activation of cdk4. Forced induction of cyclin D1 in myotubes results in the cytoplasmic to nuclear translocation of cdk4. The specific MyoD-cdk4 interaction in dividing myoblasts, coupled with the cyclin D1-dependent nuclear targeting of cdk4, suggests a mitogen-sensitive mechanism whereby cyclin D1 can regulate MyoD function and the onset of myogenesis by controlling the cellular location of cdk4 rather than the phosphorylation status of MyoD.  (+info)

Ral-specific guanine nucleotide exchange factor activity opposes other Ras effectors in PC12 cells by inhibiting neurite outgrowth. (6/24243)

Ras proteins can activate at least three classes of downstream target proteins: Raf kinases, phosphatidylinositol-3 phosphate (PI3) kinase, and Ral-specific guanine nucleotide exchange factors (Ral-GEFs). In NIH 3T3 cells, activated Ral-GEFs contribute to Ras-induced cell proliferation and oncogenic transformation by complementing the activities of Raf and PI3 kinases. In PC12 cells, activated Raf and PI3 kinases mediate Ras-induced cell cycle arrest and differentiation into a neuronal phenotype. Here, we show that in PC12 cells, Ral-GEF activity acts opposite to other Ras effectors. Elevation of Ral-GEF activity induced by transfection of a mutant Ras protein that preferentially activates Ral-GEFs, or by transfection of the catalytic domain of the Ral-GEF Rgr, suppressed cell cycle arrest and neurite outgrowth induced by nerve growth factor (NGF) treatment. In addition, Rgr reduced neurite outgrowth induced by a mutant Ras protein that preferentially activates Raf kinases. Furthermore, inhibition of Ral-GEF activity by expression of a dominant negative Ral mutant accelerated cell cycle arrest and enhanced neurite outgrowth in response to NGF treatment. Ral-GEF activity may function, at least in part, through inhibition of the Rho family GTPases, CDC42 and Rac. In contrast to Ras, which was activated for hours by NGF treatment, Ral was activated for only approximately 20 min. These findings suggest that one function of Ral-GEF signaling induced by NGF is to delay the onset of cell cycle arrest and neurite outgrowth induced by other Ras effectors. They also demonstrate that Ras has the potential to promote both antidifferentiation and prodifferentiation signaling pathways through activation of distinct effector proteins. Thus, in some cell types the ratio of activities among Ras effectors and their temporal regulation may be important determinants for cell fate decisions between proliferation and differentiation.  (+info)

The abundance of cell cycle regulatory protein Cdc4p is controlled by interactions between its F box and Skp1p. (7/24243)

Posttranslational modification of a protein by ubiquitin usually results in rapid degradation of the ubiquitinated protein by the proteasome. The transfer of ubiquitin to substrate is a multistep process. Cdc4p is a component of a ubiquitin ligase that tethers the ubiquitin-conjugating enzyme Cdc34p to its substrates. Among the domains of Cdc4p that are crucial for function are the F-box, which links Cdc4p to Cdc53p through Skp1p, and the WD-40 repeats, which are required for binding the substrate for Cdc34p. In addition to Cdc4p, other F-box proteins, including Grr1p and Met30p, may similarly act together with Cdc53p and Skp1p to function as ubiquitin ligase complexes. Because the relative abundance of these complexes, known collectively as SCFs, is important for cell viability, we have sought evidence of mechanisms that modulate F-box protein regulation. Here we demonstrate that the abundance of Cdc4p is subject to control by a peptide segment that we term the R-motif (for "reduced abundance"). Furthermore, we show that binding of Skp1p to the F-box of Cdc4p inhibits R-motif-dependent degradation of Cdc4p. These results suggest a general model for control of SCF activities.  (+info)

Induced expression of p16(INK4a) inhibits both CDK4- and CDK2-associated kinase activity by reassortment of cyclin-CDK-inhibitor complexes. (8/24243)

To investigate the mode of action of the p16(INK4a) tumor suppressor protein, we have established U2-OS cells in which the expression of p16(INK4a) can be regulated by addition or removal of isopropyl-beta-D-thiogalactopyranoside. As expected, induction of p16(INK4a) results in a G1 cell cycle arrest by inhibiting phosphorylation of the retinoblastoma protein (pRb) by the cyclin-dependent kinases CDK4 and CDK6. However, induction of p16(INK4a) also causes marked inhibition of CDK2 activity. In the case of cyclin E-CDK2, this is brought about by reassortment of cyclin, CDK, and CDK-inhibitor complexes, particularly those involving p27(KIP1). Size fractionation of the cellular lysates reveals that a substantial proportion of CDK4 participates in active kinase complexes of around 200 kDa. Upon induction of p16(INK4a), this complex is partly dissociated, and the majority of CDK4 is found in lower-molecular-weight fractions consistent with the formation of a binary complex with p16(INK4a). Sequestration of CDK4 by p16(INK4a) allows cyclin D1 to associate increasingly with CDK2, without affecting its interactions with the CIP/KIP inhibitors. Thus, upon the induction of p16(INK4a), p27(KIP1) appears to switch its allegiance from CDK4 to CDK2, and the accompanying reassortment of components leads to the inhibition of cyclin E-CDK2 by p27(KIP1) and p21(CIP1). Significantly, p16(INK4a) itself does not appear to form higher-order complexes, and the overwhelming majority remains either free or forms binary associations with CDK4 and CDK6.  (+info)

The Birt-Hogg-Dube disease occurs as a result of germline mutations in the human Folliculin gene (FLCN), and is characterized by clinical features including fibrofolliculomas, lung cysts and multifocal renal neoplasia. Clinical and genetic evidence suggest that FLCN acts as a tumor suppressor gene. The human cell line UOK257, derived from the renal cell carcinoma of a patient with a germline mutation in the FLCN gene, harbors a truncated version of the FLCN protein. Reconstitution of the wild type FLCN protein into UOK257 cells delays cell cycle progression, due to a slower progression through the late S and G2/M-phases. Similarly, Flcn-/- mouse embryonic fibroblasts progress more rapidly through the cell cycle than wild type controls (Flcnflox/flox). The reintroduction of tumor-associated FLCN mutants (FLCN DF157, FLCN 1-469 or FLCN K508R) fails to delay cell cycle progression in UOK257 cells. Additionally, FLCN phosphorylation (on Serines 62 and 73) fluctuates throughout the cell cycle and ...
The retinoblastoma protein: Rb) inhibits both cell division and apoptosis, but the mechanism by which Rb alternatively regulates these divergent outcomes remains poorly understood. Cyclin dependent kinases: Cdks) promote cell division by phosphorylating and reversibly inactivating Rb by a hierarchical series of phosphorylation events and sequential conformational changes. The stress-regulated mitogen activated protein kinase: MAPK) p38 also phosphorylates Rb, but it does so in a cell cycle-independent manner that is associated with apoptosis rather than with cell division. Here, we show that p38 phosphorylates Rb by a novel mechanism that is distinct from that of Cdks. p38 bypasses the cell cycle-associated hierarchical phosphorylation and directly phosphorylates Rb on Ser567, which is not phosphorylated during the normal cell cycle. Phosphorylation by p38, but not Cdks, triggers an interaction between Rb and the human homologue of murine double minute 2: Hdm2), leading to degradation of Rb, release of
Rice (Oryza sativa L.) as a model and crop plant with a sequenced genome offers an outstanding experimental system for discovering and functionally analyzing the major cell cycle control elements in a cereal species. In this study, we identified the core cell cycle genes in the rice genome through a hidden Markov model search and multiple alignments supported with the use of short protein sequence probes. In total we present 55 rice putative cell cycle genes with locus identity, chromosomal location, approximate chromosome position and EST accession number. These cell cycle genes include nine cyclin dependent-kinase (CDK) genes, 27 cyclin genes, one CKS gene, two RBR genes, nine E2F/DP/DEL genes, six KRP genes, and one WEE gene. We also provide characteristic protein sequence signatures encoded by CDK and cyclin gene variants. Promoter analysis by the FootPrinter program discovered several motifs in the regulatory region of the core cell cycle genes. As a first step towards functional ...
TY - JOUR. T1 - High-resolution timing of cell cycle-regulated gene expression. AU - Rowicka-Kudlicka, Malgorzata. AU - Kudlicki, Andrzej. AU - Tu, Benjamin P.. AU - Otwinowski, Zbyszek. PY - 2007/10/23. Y1 - 2007/10/23. N2 - The eukaryotic cell division cycle depends on an intricate sequence of transcriptional events. Using an algorithm based on maximum-entropy deconvolution, and expression data from a highly synchronized yeast culture, we have timed the peaks of expression of transcriptionally regulated cell cycle genes to an accuracy of 2 min (≈1% of the cell cycle time). The set of 1,129 cell cycle-regulated genes was identified by a comprehensive analysis encompassing all available cell cycle yeast data sets. Our results reveal distinct subphases of the cell cycle undetectable by morphological observation, as well as the precise timeline of macromolecular complex assembly during key cell cycle events.. AB - The eukaryotic cell division cycle depends on an intricate sequence of ...
Retinoids have antiproliferative effects in human breast cancer cells and share some characteristics with antiestrogens, although the molecular targets involved have yet to be identified in either case. Using T-47D human breast cancer cells, we compared the effects of retinoic acid (RA) and the antiestrogen ICI 164384 on cell cycle phase distribution and the expression of genes with known functions in cell cycle control. Both RA and ICI 164384 inhibited cell cycle progression in G1 phase, but the RA effect was delayed by 16 h. This delay in action was also seen with 9-cis RA and other retinoids. Administration of 17 beta-estradiol abolished the effects of ICI 164384 but was without effect in RA-treated cells. Antiestrogen treatment caused a rapid inhibition of c-myc and cyclin D1 gene expression and reduced Cdk2 activity by more than 50% at 24 h. RA, however, did not affect c-myc or cyclin D1 gene expression, nor did it significantly change the mRNA or protein levels of cyclins D3 or E or cyclin
Combinations of gemcitabine and trabectedin exert modest synergistic cytotoxic effects on two pancreatic cancer cell lines. Here, systems pharmacodynamic (PD) models that integrate cellular response data and extend a prototype model framework were developed to characterize dynamic changes in cell cycle phase of cancer cell subpopulations in response to gemcitabine and trabectedin as single agents and in combination. Extensive experimental data were obtained for two pancreatic cancer cell lines (MiaPaCa-2 and BxPC-3), including cell proliferation rates over 0-120 h of drug exposure, and the fraction of cells in different cell cycle phases or apoptosis. Cell cycle analysis demonstrated that gemcitabine induced cell cycle arrest in S phase, and trabectedin induced transient cell cycle arrest in S phase that progressed to G2/M phase. Over time, cells in the control group accumulated in G0/G1 phase. Systems cell cycle models were developed based on observed mechanisms and were used to characterize both cell
The cell cycle includes 4 main phases: Gap 1 (G1), DNA replication (S), Gap 2 (G2), and mitosis (M). Tight regulation of the transition between these phases halts cell cycle progression if a phase is not properly completed. For example, the G2-M DNA damage checkpoint ensures the fidelity of DNA replication, and arrests the cell cycle to allow time for replication error correction and DNA damage repair. Cell cycle progression is regulated by the cyclic rise and fall of kinase expression, and their interaction with, and action on, their cyclin targets. Cell cycle dysregulation commonly occurs during oncogenesis, and tumor cells often do not arrest the cell cycle when normally required. Key genes that regulate cell cycle progression and checkpoints encode cullins, cyclins, and cyclin-dependent kinases and their inhibitors. Other cell cycle regulatory genes include apoptosis regulators and DNA damage sensors ...
Jang S.W., Liu X., Fu H., Rees H., Yepes M., Levey A., Ye K.. Terminally differentiated neurons are unable to reenter the cell cycle. Aberrant cell cycle activation provokes neuronal cell death, whereas cell cycle inhibition elevates neuronal survival. However, the molecular mechanism regulating the cell cycle and cell death in mature neurons remains elusive. Here we show that SRPK2, a protein kinase specific for the serine/arginine (SR) family of splicing factors, triggers cell cycle progression in neurons and induces apoptosis through regulation of nuclear cyclin D1. Akt phosphorylates SRPK2 on Thr-492 and promotes its nuclear translocation leading to cyclin D1 up-regulation, cell cycle reentry, and neuronal apoptosis. In addition, SRPK2 phosphorylates SC35 and, thus, inactivates p53, resulting in cyclin D1 up-regulation. 14-3-3 binding to SRPK2, regulated by Akt phosphorylation, inhibits these events. We find that SRPK2 is phosphorylated in ischemia-attacked brain, correlating with the ...
TY - CHAP. T1 - Myocardial regeneration via cell cycle activation. AU - LaFontant, Pascal J.. AU - Field, Loren J.. PY - 2007/1/1. Y1 - 2007/1/1. N2 - Introduction During development, increases in heart size results as a consequence of the differentiation and proliferation of cardiomyocytes, neurons, interstitial cells, and components of the vasculature. At birth, cardiomyocytes undergo a gradual transition from hyperplastic to hypertrophic growth, such that subsequent increases in myocardial mass result largely from increased myocyte size rather than increased number. In contrast, the other cell types present in the heart retain the ability to proliferate. Consequently, in adults, although cardiomyocytes constitute approximately 90% of the mass of the heart, they constitute less than 20% of the total number of cells present.. AB - Introduction During development, increases in heart size results as a consequence of the differentiation and proliferation of cardiomyocytes, neurons, interstitial ...
The Cell Cycle Ontology ( ) is an application ontology that automatically captures and integrates detailed knowledge on the cell cycle process. Cell Cycle Ontology is enabled by semantic web technologies, and is accessible via the web for browsing, visualizing, advanced querying, and computational reasoning. Cell Cycle Ontology facilitates a detailed analysis of cell cycle-related molecular network components. Through querying and automated reasoning, it may provide new hypotheses to help steer a systems biology approach to biological network building.
TY - JOUR. T1 - Double blockade of cell cycle at G1-S transition and M phase by 3-iodoacetamido benzoyl ethyl ester, a new type of tubulin ligand. AU - Jiang, Jian Dong. AU - Denner, Larry. AU - Ling, Yi He. AU - Li, Jian Nong. AU - Davis, Ashley. AU - Wang, Yue. AU - Li, Yan. AU - Roboz, Julia. AU - Wang, Long Gui. AU - Perez-Soler, Roman. AU - Marcelli, Marco. AU - Bekesi, George. AU - Holland, James F.. PY - 2002. Y1 - 2002. N2 - 3-Iodoacetamido benzoyl ethyl ester (3-IAABE) is a new compound synthesized in our laboratory. The primary action of 3-IAABE is to inhibit microtubule assembly by interacting with -SH groups on tubulin. In contrast to other known microtubule disrupters, 3-IAABE caused a double blockade in the cell cycle at G1-S transition and in M phase. The blockade was determined by cell cycle analysis and chromosome distribution. Kinase activities of cyclin E and cyclin-dependent kinase 2 responsible for the G1-S transition were increased, as were the activities of mitotic cyclin ...
Pluripotency and the capability for self-renewal are essential characteristics of human embryonic stem cells (hESCs), which hold great potential as a cellular source for tissue replacement. Short cell cycle (15-16 h) compared to somatic cells is another property of hESCs. Efficient synchronization of hESCs at different cell cycle stages is important to elucidate the mechanistic link between cell cycle regulation and cell fate decision. This protocol describes how to establish synchronization of hESCs at different cell cycle stages.
TY - JOUR. T1 - A cell cycle study of the effects of Con A on synchronized mouse embryo fibroblasts. T2 - Arrest and dissociation between uptake of thymidine and DNA synthesis. AU - Mallucci, L.. AU - Dunn, M.. AU - Wells, V.. AU - Delia, D.. PY - 1980. Y1 - 1980. N2 - We have examined the effects of 50 μg ml-1 of Con A added to synchronized mouse embryo fibroblasts at different times during the cell cycle. We found that Con A caused arrest of growth not solely by preventing G1-G0 cells from entering the S-phase but also by exerting a G2 block. We also found that Con A, which prevented commencement of S-phase, did not arrest cells already in S from reaching the G2 stage but inhibited the S-phase associated process of thymidine uptake. The inhibition was greater when the Con A receptors were extensively clustered.. AB - We have examined the effects of 50 μg ml-1 of Con A added to synchronized mouse embryo fibroblasts at different times during the cell cycle. We found that Con A caused arrest of ...
During the cell division cycle of the yeast Saccharomyces cerevisiae, the G1-to-S transition depends upon the activation of two transcription factors (SBF and MBF), which are responsible for the cell cycle-regulated expression of more than 200 genes. Bck2 becomes essential in the absence of Cln3, the most upstream activator of this transcriptional program. Here we have used a genome-wide approach to elucidate the targets of Bck2. Our data indicate that Bck2 activates a selection of cell cycle-regulated genes from all cell cycle stages. In contrast, Cln3 activates only G1/S phase genes. Furthermore, Bck2 activates many genes independently of Swi6, the common component of SBF and MBF. Comparison of Bck2 targets with those of other transcription factors suggests that, in addition to SBF and MBF, Bck2 may elicit gene expression via Ste12 and Mcm1. We propose that Bck2 activates its targets by a mechanism fundamentally different from that of Cln3, and that it may be a necessary cofactor for the full ...
Time-course microarray experiments have been widely used to identify cell cycle regulated genes. However, the method is not effective for lowly expressed genes and is sensitive to experimental conditions. To complement microarray experiments, we propose a computational method to predict cell cycle regulated genes based on their genomic features - transcription factor binding and motif profiles. Through integrating gene-expression data with ChIP-chip binding and putative binding sites of transcription factors, our method shows high accuracy in discriminating yeast cell cycle regulated genes from non-cell cycle regulated ones. We predict 211 novel cell cycle regulated genes. Our model rediscovers the main cell cycle transcription factors and provides new insights into the regulatory mechanisms. The model also reveals a regulatory circuit mediated by a number of key cell cycle regulators. Our model suggests that the periodical pattern of cell cycle genes is largely coded in their promoter regions, which
TY - JOUR. T1 - Multiple nuclei tracking using integer programming for quantitative cancer cell cycle analysis. AU - Li, Fuhai. AU - Zhou, Xiaobo. AU - Ma, Jinwen. AU - Wong, Stephen T C. PY - 2010/1. Y1 - 2010/1. N2 - Automated cell segmentation and tracking are critical for quantitative analysis of cell cycle behavior using time-lapse fluorescence microscopy. However, the complex, dynamic cell cycle behavior poses new challenges to the existing image segmentation and tracking methods. This paper presents a fully automated tracking method for quantitative cell cycle analysis. In the proposed tracking method, we introduce a neighboring graph to characterize the spatial distribution of neighboring nuclei, and a novel dissimilarity measure is designed based on the spatial distribution, nuclei morphological appearance, migration, and intensity information. Then, we employ the integer programming and division matching strategy, together with the novel dissimilarity measure, to track cell nuclei. We ...
PURPOSE The cell cycle progression test is a validated molecular assay that assesses prostate cancer specific disease progression and mortality risk when combined with clinicopathological parameters. We present the results from PROCEDE-1000, a large, prospective registry designed to evaluate the impact of the cell cycle progression test on shared treatment decision making for patients newly diagnosed with prostate cancer. MATERIALS AND METHODS Untreated patients with newly diagnosed prostate adenocarcinoma were enrolled in the study and the cell cycle progression test was performed on the initial prostate biopsy tissue. A set of 4 sequential surveys tracked changes relative to initial therapy recommendations (before cell cycle progression) based on clinicopathological parameters following physician review of the cell cycle progression test result, physician/patient review of the cell cycle progression test results and a minimum of 3 months of clinical followup (actual treatment). RESULTS Of the 1
TY - JOUR. T1 - Association of cell cycle expression of Ia-like antigenic determinants on normal human multipotential (CFU-GEMM) and erythroid (BFU-E) progenitor cells with regulation in vitro by acidic isoferritins. AU - Lu, L.. AU - Broxmeyer, H. E.. AU - Meyers, P. A.. AU - Moore, M. A.. AU - Thaler, H. T.. PY - 1983. Y1 - 1983. N2 - An association has been established between human Ia-like antigenic determinants, expression during DNA synthesis on multipotential (CFU-GEMM) and erythroid (BFU-E) progenitor cells, and the regulatory action of acidic isoferritins in vitro. Treatment of human bone marrow cells with monoclonal anti-Ia (NE1-011) plus complement inhibited colony formation of CFU-GEMM and BFU-E by 50%-70%. Reduction of colonies was similar whether bone marrow cells were exposed to anti-Ia plus complement, high specific activity tritiated thymidine (3HTdr), or acidic isoferritins. No further decrease was apparent with 3HTdr or acidic isoferritins after Ia-antigen+ CFU-GEMM or BFU-E ...
Cell Growth and Reproduction Study Guide The Cell Cycle Study Guide Vocabulary - Cell Cycle, Mitosis, Cytokinesis 1. How did the G1 and G2 stages get their
Successful progression through the cell cycle requires spatial and temporal regulation of gene transcript levels and the number, positions and condensation levels of chromosomes. Here we present a high resolution survey of genome interactions in Schizosaccharomyces pombe using synchronized cells to investigate cell cycle dependent changes in genome organization and transcription. Cell cycle dependent interactions were captured between and within S. pombe chromosomes. Known features of genome organization (e.g. the clustering of telomeres and retrotransposon long terminal repeats (LTRs)) were observed throughout the cell cycle. There were clear correlations between transcript levels and chromosomal interactions between genes, consistent with a role for interactions in transcriptional regulation at specific stages of the cell cycle. In silico reconstructions of the chromosome organization within the S. pombe nuclei were made by polymer modeling. These models suggest that groups of genes with high ...
Geminiviruses are small DNA viruses that use plant replication machinery to amplify their genomes. Microarray analysis of the Arabidopsis (Arabidopsis thaliana) transcriptome in response to cabbage leaf curl virus (CaLCuV) infection uncovered 5,365 genes (false discovery rate ,0.005) differentially expressed in infected rosette leaves at 12 d postinoculation. Data mining revealed that CaLCuV triggers a pathogen response via the salicylic acid pathway and induces expression of genes involved in programmed cell death, genotoxic stress, and DNA repair. CaLCuV also altered expression of cell cycle-associated genes, preferentially activating genes expressed during S and G2 and inhibiting genes active in G1 and M. A limited set of core cell cycle genes associated with cell cycle reentry, late G1, S, and early G2 had increased RNA levels, while core cell cycle genes linked to early G1 and late G2 had reduced transcripts. Fluorescence-activated cell sorting of nuclei from infected leaves revealed a ...
The cell cycle is central to understanding fundamental biology of Leishmania, a group of human-infective protozoan parasites. Leishmania have two main life cycle morphologies: the intracellular amastigote in the mammalian host and the promastigote in the fly. We have produced the first comprehensive and quantitative description of a Leishmania promastigote cell cycle taking a morphometric approach to position any cell within the cell cycle based on its length and DNA content. We describe timings of cell cycle phases and rates of morphological changes; kinetoplast and nucleus S phase, division and position, cell body growth and morphology changes, flagellum growth and basal body duplication. We have shown that Leishmania mexicana undergoes large changes in morphology through the cell cycle and that the wide range of morphologies present in cultures during exponential growth represent different cell cycle stages. We also show promastigote flagellum growth occurs over multiple cell cycles. There are clear
Live fast, die soon: cell cycle progression and lifespan in yeast cells - Our understanding of lifespan has benefited enormously from the study of a simple model, the yeast Saccharomyces cerevisiae. Although a unicellular organism, yeasts undergo many of the processes directly related with aging that to some extent are conserved in mammalian cells. Nutrient-limiting conditions have been involved in lifespan extension, especially in the case of caloric restriction, which also has a direct impact on cell cycle progression. In fact, other environmental stresses (osmotic, oxidative) that interfere with normal cell cycle progression also influence the lifespan of cells, indicating a relationship between lifespan and cell cycle control. In the present review we compile and discuss new findings related to how cell cycle progression is regulated by other nutrients. We centred this review on the analysis of phosphate, also give some attention to nitrogen, and the impact of these nutrients on lifespan...
Distinct patterns of histone methylation during human cell cycle progression are described. Histone H4 methyltransferase activity is cell cycle-regulated, consistent with increased H4 Lys 20 methylation at mitosis. This increase closely follows the cell cycle-regulated expression of the H4 Lys 20 methyltransferase, PR-Set7. Localization of PR-Set7 to mitotic chromosomes and subsequent increase in H4 Lys 20 methylation were inversely correlated to transient H4 Lys 16 acetylation in early S-phase. These data suggest that H4 Lys 20 methylation by PR-Set7 during mitosis acts to antagonize H4 Lys 16 acetylation and to establish a mechanism by which this mark is epigenetically transmitted (Rice, 2002). To determine histone methyltransferase activity during the human cell cycle, HeLa cells were arrested by treatment with thymidine followed by mimosine. Every 2.5 h following release from the G1 arrest, synchronized cells were isolated for analysis, and the cell cycle phase was determined by ...
Despite traditionally regarded as identical, cells in a microbial cultivation present a distribution of phenotypic traits, forming a heterogeneous cell population. Moreover, the degree of heterogeneity is notably enhanced by changes in micro-environmental conditions. A major development in experimental single-cell studies has taken place in the last decades. It has however not been fully accompanied by similar contributions within data analysis and mathematical modeling. Indeed, literature reporting, for example, quantitative analyses of experimental single-cell observations and validation of model predictions for cell property distributions against experimental data is scarce. This study focuses on the experimental and mathematical description of the dynamics of cell size and cell cycle position distributions, of a population of Saccharomyces cerevisiae, in response to the substrate consumption observed during batch cultivation. The good agreement between the proposed multi-scale model (a ...
A recent in-depth view of cell cycle regulation and cancer has provided novel samples of research at the Frontiers of Science. However, the number of foremost revealing information about both the topics has been derived from the intersection of these two fields.1-5 This review intends to introduce the basics of the cell cycle and its regulation at different checkpoints in relation to cancer. Cancer is broadly a result of unchecked cell multiplication due to abnormal activity of varied cell cycle proteins; therefore, cell cycle regulators are considered attractive targets in cancer therapy. Many cancers are uniquely linked with these proteins and are therefore selectively sensitive to their inhibition.6 After a long run of research on the physiological functions of cell cycle proteins and their relevance for cancer, these data recently got converted into the first approved cancer therapeutics, targeting the regulator of cell cycle.7 Here, we are reviewing the role of cell cycle proteins in ...
NADPH oxidase 2 (Nox2)-derived oxidative stress and redox-signalling have been found to play an important role in hyperglycaemia-induced endothelial dysfunction in diabetes. Acetate (NaA) is a member of the short chain fatty acids (SCFA) family which acts through G-protein coupled receptor 43 (GPCR43) to exert anti-inflammatory effects and to increase insulin sensitivity. However, its action in endothelial cells remains unknown. In this study we investigated the effects of NaA and GPCR43 on high glucose (30 mM, 24 h)-induced Nox2 activation and endothelial cell cycle progression using human pulmonary microvascular endothelial cells (HPMECs). Compared to control cells, high glucose increased significantly i) Nox2-derived superoxide production (48.5±12.6%) as detected by both lucigenin (5 µM)-chemiluminescence and DHE fluorescence; ii) expression of cyclin D, A and E and cell cycle progression from G0/G1 to S and G2/M phases and iii) cell apoptosis (30.66±8.3%) (all p,0.05). These high-glucose ...
The neocortex is patterned in layers of neurons that are generated in an orderly sequence during development. This correlation between cell birthday and laminar fate prompted an examination of how neuronal phenotypes are determined in the developing cortex. At various times after labeling with [3H]thymidine, embryonic progenitor cells were transplanted into older host brains. The laminar fate of transplanted neurons correlates with the position of their progenitors in the cell cycle at the time of transplantation. Daughters of cells transplanted in S-phase migrate to layer 2/3, as do host neurons. Progenitors transplanted later in the cell cycle, however, produce daughters that are committed to their normal, deep-layer fates. Thus, environmental factors are important determinants of laminar fate, but embryonic progenitors undergo cyclical changes in their ability to respond to such cues. ...
TY - JOUR. T1 - ZNF313 is a novel cell cycle activator with an E3 ligase activity inhibiting cellular senescence by destabilizing p21WAF1. AU - Han, J.. AU - Kim, Y. L.. AU - Lee, K. W.. AU - Her, N. G.. AU - Ha, T. K.. AU - Yoon, S.. AU - Jeong, S. I.. AU - Lee, J. H.. AU - Kang, M. J.. AU - Lee, M. G.. AU - Ryu, B. K.. AU - Baik, J. H.. AU - Chi, S. G.. PY - 2013/8. Y1 - 2013/8. N2 - ZNF313 encoding a zinc-binding protein is located at chromosome 20q13.13, which exhibits a frequent genomic amplification in multiple human cancers. However, the biological function of ZNF313 remains largely undefined. Here we report that ZNF313 is an ubiquitin E3 ligase that has a critical role in the regulation of cell cycle progression, differentiation and senescence. In this study, ZNF313 is initially identified as a XIAP-associated factor 1 (XAF1)-interacting protein, which upregulates the stability and proapoptotic effect of XAF1. Intriguingly, we found that ZNF313 activates cell cycle progression and ...
For many organisms, the first goal of embryogenesis is to accumulate a large cell population to accommodate gastrulation. To achieve this quickly, embryos employ specialized cell cycles called cleavages that consist of continuous rounds of DNA replication and division. Cell proliferation occurs rapidly because cleavage cycles lack the gap phases and cell cycle checkpoints found in canonical cell cycles. Further, the genetic materials required to sustain cleavage cycles are preloaded during oogenesis, aiding efficient cell cycle progression. After a constant, organism-specific number of cleavages, many metazoan embryos undergo the mid-blastula transition (MBT), which initiates extensive cell cycle remodeling. Cell cycles lengthen, gap phases appear and checkpoint function is acquired. At the same time, the nearly quiescent zygotic genome is activated and transcriptional activity dramatically increases. This dissertation describes how these simultaneous MBT events are regulated. Chapter 2 addresses how
CYCD3;1 expression in Arabidopsis is associated with proliferating tissues such as meristems and developing leaves but not with differentiated tissues. Constitutive overexpression of CYCD3;1 increases CYCD3;1-associated kinase activity and reduces the proportion of cells in the G1-phase of the cell cycle. Moreover, CYCD3;1 overexpression leads to striking alterations in development. Leaf architecture in overexpressing plants is altered radically, with a failure to develop distinct spongy and palisade mesophyll layers. Associated with this, we observe hyperproliferation of leaf cells; in particular, the epidermis consists of large numbers of small, incompletely differentiated polygonal cells. Endoreduplication, a marker for differentiated cells that have exited from the mitotic cell cycle, is inhibited strongly in CYCD3;1-overexpressing plants. Transcript analysis reveals an activation of putative compensatory mechanisms upon CYCD3;1 overexpression or subsequent cell cycle activation. These ...
Cell proliferation is essential for many key processes that occur during development including organogenesis, tissue renewal and germline formation. (Bartkova et al., 1997; Clurman and Roberts, 1995; Pines, 1995; Sandhu and Slingerland, 2000). Therefore, the timing of cell division and differentiation must be precisely coordinated with signals that specify morphogenesis, patterning and growth in a temporal, positional and cell type-specific manner (reviewed by Vidwans and Su, 2001). This coordination is executed through regulating both positive and negative regulatory components of the basal cell cycle machinery.. The cell cycle machinery is well conserved among eukaryotes and complex mechanisms ensure that cell cycle progression occurs in a timely and precise sequence. Cyclin-dependent kinases (Cdks) drive progression through the different cell cycle phases (reviewed by Nigg, 2001). In yeasts, these catalytic subunits are regulated through their association with stage-specific cyclin regulatory ...
Activation of growth factor receptors by ligand binding initiates a cascade of events leading to cell growth and division. Progression through the cell cycle is controlled by cyclin-dependent protein kinases (Cdks), but the mechanisms that link growth factor signaling to the cell cycle machinery have not been established. We report here that Ras proteins play a key role in integrating mitogenic signals with cell cycle progression through G1. Ras is required for cell cycle progression and activation of both Cdk2 and Cdk4 until approximately 2 h before the G1/S transition, corresponding to the restriction point. Analysis of Cdk-cyclin complexes indicates that Ras signaling is required both for induction of cyclin D1 and for downregulation of the Cdk inhibitor p27KIP1. Constitutive expression of cyclin D1 circumvents the requirement for Ras signaling in cell proliferation, indicating that regulation of cyclin D1 is a critical target of the Ras signaling cascade. ...
TY - JOUR. T1 - Rapamycin blocks IL-2-driven T cell cycle progression while preserving T cell survival. AU - Gonzalez, Juana. AU - Harris, Tom. AU - Childs, Geoffrey. AU - Prystowsky, Michael B.. PY - 2001/1/1. Y1 - 2001/1/1. N2 - Effective cellular immune responses require increases in antigen-specific T lymphocytes; IL-2 drives antigen-stimulated T cell proliferation and is largely responsible for the increases observed. We used microarrays containing ∼9000 mouse cDNAs to study IL-2-induced gene expression. IL-2 induces the expression of genes that regulate cell cycle progression, control cell survival, and increase synthetic and metabolic processes during proliferation. IL-2 also suppresses expression of genes that block cell cycle progression and promote cell death. Rapamycin inhibits IL-2-driven proliferation by downregulating the expression of genes required for key processes required for cell cycle progression. Rapamycin also preserves cell survival by keeping intact the IL-2-induced ...
TY - JOUR. T1 - Cell-size dependent progression of the cell cycle creates homeostasis and flexibility of plant cell size. AU - Jones, Angharad R.. AU - Forero-Vargas, Manuel. AU - Withers, Simon P.. AU - Smith, Richard S.. AU - Traas, Jan. AU - Dewitte, Walter. AU - Murray, James A.H.. PY - 2017/1/1. Y1 - 2017/1/1. N2 - © The Author(s) 2017. Mean cell size at division is generally constant for specific conditions and cell types, but the mechanisms coupling cell growth and cell cycle control with cell size regulation are poorly understood in intact tissues. Here we show that the continuously dividing fields of cells within the shoot apical meristem of Arabidopsis show dynamic regulation of mean cell size dependent on developmental stage, genotype and environmental signals. We show cell size at division and cell cycle length is effectively predicted using a two-stage cell cycle model linking cell growth and two sequential cyclin dependent kinase (CDK) activities, and experimental results concur ...
Cell proliferation is the main driving force for plant growth. Although genome sequence analysis revealed a high number of cell cycle genes in plants, little is known about the molecular complexes steering cell division. In a targeted proteomics approach, we mapped the core complex machinery at the heart of the Arabidopsis thaliana cell cycle control. Besides a central regulatory network of core complexes, we distinguished a peripheral network that links the core machinery to up- and downstream pathways. Over 100 new candidate cell cycle proteins were predicted and an in-depth biological interpretation demonstrated the hypothesis-generating power of the interaction data. The data set provided a comprehensive view on heterodimeric cyclin-dependent kinase (CDK)cyclin complexes in plants. For the first time, inhibitory proteins of plant-specific B-type CDKs were discovered and the anaphase-promoting complex was characterized and extended. Important conclusions were that mitotic A- and B-type ...
The cell cycle proteins are key regulators of cell cycle progression whose de-regulation is one of the causes of breast cancer. RNA interference (RNAi) is an endogenous mechanism to regulate gene expression and it could serve as the basis of regulating aberrant proteins including cell cycle proteins. Since the delivery of small interfering RNA (siRNA) is a main barrier for implementation of RNAi therapy, we explored the potential of a non-viral delivery system, 2.0 kDa polyethylenimines substituted with linoleic acid and caprylic acid, for this purpose. Using a library of siRNAs against cell cycle proteins, we identified cell division cycle protein 20 (CDC20), a recombinase RAD51, and serine-threonine protein kinase CHEK1 as effective targets for breast cancer therapy, and demonstrated their therapeutic potential in breast cancer MDA-MB-435, MDA-MB-231 and MCF7 cells with respect to another well-studied cell cycle protein, kinesin spindle protein. We also explored the efficacy of dicer-substrate siRNA
In recent years, increasing research has focused on the relationship between cytokines and tumorigenesis. It has been suggested that cytokines may be a new therapeutic option for tumors (16-20). In our experiments, we demonstrated that IFN-λ1 inhibited the growth of gastric carcinoma cells in a concentration-dependent manner. These data suggest that IFN-λ1 may be a potential antitumor agent for the treatment of gastric cancer.. Impaired apoptotic induction and dysregulated cell cycle progression are important factors in cancer development. Accordingly, inhibition of cell cycle regulation is particularly useful in the treatment of cancer. In our in vitro study, we demonstrated the apoptosis-inducing effects of IFN-λ1 in gastric carcinoma cells using PI cell cycle analysis, Annexin V and PI staining as well as activated caspase-3. Our study showed that IFN-λ1 induced G1 phase arrest and apoptosis in the gastric carcinoma cells.. Experimental evidence suggests that apoptosis can be mediated by ...
Tumor cells stably transfected with fluorescent proteins enable scientists to visualize many important aspects of cancer in real time at the single cell level. For example, transfected tumor cells have been visualized either through surgically created chronic-transparent windows or directly through the opened skin of living animals [29]. This intravital imaging provides a powerful tool for observing cancer initiation and progression and evaluating the efficacy of candidate cancer drugs in vivo. On the other hand, assays using tumor cells grown in culture provide reliable information about cancer mechanisms, and are amenable to automated high-throughput screening [16-20]. Using a modified fluorescent indicator of cell cycle progression (Fucci2) and cultured immortalized cells, we investigated the mechanism(s) by which anticancer drugs modulate the cell cycle. While population analysis provided statistical data, time-lapse high-resolution imaging analysis allowed us to explore the processes of ...
Proper DNA replication and well-timed cell cycle progression are vital to the normal functioning of a cell. Precise coordination between these mechanisms constituent proteins ensures their processivity while safeguarding against DNA damage. The Ctf4 protein is a central member of the replication fork and links the replicative MCM helicase and polymerase [alpha]-primase. In addition, it has been implicated as a member of a complex that promotes replication fork stability, the Fork Protection Complex (FPC). This investigation represents the first phenotypic analysis of the function of the Ctf4 protein within a multicellular organism model. We show that Ctf4 interacts with Polymerase [alpha], MCM2, Psf1, and Psf2. We also demonstrate that knockdown of this central replication fork component via a GAL4-UAS RNAi system results in a lower frequency of mitosis due to an S-phase delay, endoreplication defects, as well as mitotic bridging in early embryonic development ...
It is widely believed that the cellular transcription factor DRTF1/E2F integrates cell cycle events with the transcription apparatus because during cell cycle progression in mammalian cells it interacts with molecules that are important regulators of cellular proliferation, suck as the retinoblastoma tumour suppressor gene product (pRb), p107, cyclins and cyclin-dependent kinases. Thus, pRb, which negatively regulates early cell cycle progression and is frequently mutated in tumour cells, and the Rb-related protein p107, bind to and repress the transcriptional activity of DRTF1/E2F. Viral oncoproteins, such as adenovirus E1a and SV40 large T antigen, overcome such repression by sequestering pRb and p107 and in so doing are likely to activate genes regulated by DRTF1/E2F, such as cdc2, c-myc and DHFR. Two sequence-specific DNA binding proteins, E2F-1 and DP-1, which bind to the E2F site, contain a small region of similarity. The functional relationship between them has, however, been unclear. We report
Mitotic cell cycle progression is accomplished through a reproducible sequence of events, DNA replication (S phase) and mitosis (M phase) separated temporally by gaps known as G1 and G2 phases. Cyclin-dependent kinases (CDKs) are key regulatory enzymes, each consisting of a catalytic CDK subunit and an activating cyclin subunit. CDKs regulate the cells progression through the phases of the cell cycle by modulating the activity of key substrates. Downstream targets of CDKs include transcription factor E2F and its regulator Rb. Precise activation and inactivation of CDKs at specific points in the cell cycle are required for orderly cell division. Cyclin-CDK inhibitors (CKIs), such as p16Ink4a, p15Ink4b, p27Kip1, and p21Cip1, are involved in the negative regulation of CDK activities, thus providing a pathway through which the cell cycle is negatively regulated. Eukaryotic cells respond to DNA damage by activating signaling pathways that promote cell cycle arrest and DNA repair. In response to DNA ...
Mitotic cell cycle progression is accomplished through a reproducible sequence of events, DNA replication (S phase) and mitosis (M phase) separated temporally by gaps known as G1 and G2 phases. Cyclin-dependent kinases (CDKs) are key regulatory enzymes, each consisting of a catalytic CDK subunit and an activating cyclin subunit. CDKs regulate the cells progression through the phases of the cell cycle by modulating the activity of key substrates. Downstream targets of CDKs include transcription factor E2F and its regulator Rb. Precise activation and inactivation of CDKs at specific points in the cell cycle are required for orderly cell division. Cyclin-CDK inhibitors (CKIs), such as p16Ink4a, p15Ink4b, p27Kip1, and p21Cip1, are involved in the negative regulation of CDK activities, thus providing a pathway through which the cell cycle is negatively regulated. Eukaryotic cells respond to DNA damage by activating signaling pathways that promote cell cycle arrest and DNA repair. In response to DNA ...
is a supervised approach for PrEdicting cell cycle phase in a COntinuum using single-cell RNA sequencing data. The R package provides functions to build training dataset and also functions to use existing training data to predict cell cycle on a continuum.. Our work demonstrated that peco is able to predict continuous cell cylce phase using a small set of cylcic genes: CDK1, UBE2C, TOP2A, HISTH1E, and HISTH1C (identified as cell cycle marker genes in studies of yeast (Spellman et al., 1998) and HeLa cells (Whitfield et al., 2002)).. Below we provide two use cases. Vignette 1 shows how to use the built-training dataset to predict continuous cell cycle. Vignette 2 shows how to make a training datast and build a predictor using training data.. Users can also view the vigenettes via ...
Video articles in JoVE about g2 phase include Cell Cycle Analysis in the C. elegans Germline with the Thymidine Analog EdU, Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols, Lineage Tracing and Clonal Analysis in Developing Cerebral Cortex Using Mosaic Analysis with Double Markers (MADM), Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis.
The centromeric histone CENP-A is incorporated at different cell cycle phases during somatic mitosis, meiosis I and meiosis II in Drosophila melanogaster.
What is Cell Cycle Gene? Definition of Cell Cycle Gene. Cell Cycle Gene FAQ. Learn more about Cell Cycle Gene. Cell Cycle Gene facts.
Cell Cycle Activity Worksheet Fresh Lifescitrc Cells Alive Mitosis Phase Worksheet one of Free Worksheets - Free, printable main idea worksheets to develop strong reading comprehension skills ideas, to explore this Cell Cycle Activity Worksheet Fresh Lifescitrc Cells Alive Mitosis Phase Worksheet idea you can browse by and . We hope your happy with this Cell Cycle Activity Worksheet Fresh Lifescitrc Cells Alive Mitosis Phase Worksheet idea. You can download and please share this Cell Cycle Activity Worksheet Fresh Lifescitrc Cells Alive Mitosis Phase Worksheet ideas to your friends and family via your social media account. Back to Cell Cycle Activity Worksheet. ...
Abstract: Modern sugarcane is an unusually complex heteroploid crop, and its genome comprises two or three subgenomes. To reduce the complexity of sugarcane genome research, the ploidy level and number of chromosomes can be reduced using flow chromosome sorting. However, a cell cycle synchronization (CCS) protocol for Saccharum spp. is needed that maximizes the accumulation of metaphase chromosomes. For flow cytometry analysis in this study, we optimized the lysis buffer, hydroxyurea(HU) concentration, HU treatment time and recovery time for sugarcane. We determined the mitotic index by microscopic observation and calculation. We found that WPB buffer was superior to other buffers for preparation of sugarcane nuclei suspensions. The optimal HU treatment was 2 mM for 18 h at 25 °C, 28 °C and 30 °C. Higher recovery treatment temperatures were associated with shorter recovery times (3.5 h, 2.5 h and 1.5 h at 25 °C, 28 °C and 30 °C, respectively). The optimal conditions for treatment with the ...
Genistein, an isoflavone, is a specific inhibitor of tyrosine kinase and topoisomerase II. However, its effect on cell growth is unknown. Therefore, we examined the effects of genistein on cell growth and cell cycle progression and compared its effects with other flavonoids. Genistein inhibited in a dose-dependent manner the growth of HGC-27 cells derived from human gastric cancer. Flow-cytometric analysis showed that genistein almost completely arrested the cell cycle progression at G2-M. This effect was reversible when genistein was removed from the culture medium. In contrast, other flavonoids such as flavone, luteolin, and the structurally similar daidzein arrested the cell cycle at G1. Consistent with the flow-cytometric analysis, microscopic observation showed that genistein did not increase the mitotic index, which supposes that genistein may arrest the cell cycle at G2 or early M. These results suggest that the G2-M arrest by genistein is a unique effect among flavonoids.. ...
Successful completion of the cell division cycle is critical for cellular duplication and survival. There are many regulators and checkpoints to ensure the proper cell cycle progression. Disruption of the machinery involved in completion, error correction, or regulation of the cell cycle can be deleterious and may lead to aberrant cell growth or cell death. Thus, it is important to understand not only the basic machinery, but also the underlying choreographed gene expression that underlies that fundamental process. The work presented in this thesis furthers our understanding of the cell cycle in three ways. First, I investigate the cell cycle-regulated transcription factor FOXM1, a gene that has been shown to play a role in the G2 to M phase transition. I show that FOXM1 is cell cycle-regulated in both HeLa and U2OS cells and that, when knocked out in synchronous HeLa cells, results in mis-regulation of select G2/M genes. I also demonstrate that FOXM1 binds to the promoters of many cell ...
Successful completion of the cell division cycle is critical for cellular duplication and survival. There are many regulators and checkpoints to ensure the proper cell cycle progression. Disruption of the machinery involved in completion, error correction, or regulation of the cell cycle can be deleterious and may lead to aberrant cell growth or cell death. Thus, it is important to understand not only the basic machinery, but also the underlying choreographed gene expression that underlies that fundamental process. The work presented in this thesis furthers our understanding of the cell cycle in three ways. First, I investigate the cell cycle-regulated transcription factor FOXM1, a gene that has been shown to play a role in the G2 to M phase transition. I show that FOXM1 is cell cycle-regulated in both HeLa and U2OS cells and that, when knocked out in synchronous HeLa cells, results in mis-regulation of select G2/M genes. I also demonstrate that FOXM1 binds to the promoters of many cell ...
Nanoparticles are considered a primary vehicle for targeted therapies because they can pass biological barriers, enter and distribute in cells by energy-dependent pathways1-3. Until now, most studies have shown that nanoparticle properties, such as size4-6 and surface7,8, can affect how cells internalise nanoparticles. Here we show that the different phases of cell growth, which constitute the cell cycle, can also influence nanoparticle uptake. Although cells in different cell cycle phases internalised nanoparticles with similar rates, after 24 hours of uptake the concentration of nanoparticles in the cells is ranked according to the different cell cycle phases: G2/M , S , G0/G1. Nanoparticles were not exported from cells but the internalised nanoparticle concentration is split when the cell divides. Our results suggest that future studies on nanoparticle uptake should consider the cell cycle because in a cell population, the internalised nanoparticle dose in each cell varies as the cell cycles ...
The unicellular green alga Chlamydomonas reinhardtii is an ideal model organism for studies of ciliary function and assembly. In assays for biological and biochemical effects of various factors on flagellar structure and function, synchronous culture is advantageous for minimizing variability. Here, we have characterized a method in which 100% synchronization is achieved with respect to flagellar length but not with respect to the cell cycle. The method requires inducing flagellar regeneration by amputation of the entire cell population and limiting regeneration time. This results in a maximally homogeneous distribution of flagellar lengths at 3 h postamputation. We found that time-limiting new protein synthesis during flagellar synchronization limits variability in the unassembled pool of limiting flagellar protein and variability in flagellar length without affecting the range of cell volumes. We also found that long- and short-flagella mutants that regenerate normally require longer and ...
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Carrageenan is a polysaccharide that exists in the cell walls of marine red algae and is widely used in studies concerned with its antitumor and cytotoxic activities [10]. Previous findings show carrageenan as a potential antitumor agent [28-30]. Considering one of the hallmarks of cancer is uncontrolled proliferation, a consequence of the loss of normal cell-cycle control, there has been a. increasing interest in potential anticancer agents that affect the cell-cycles of cancer cells [31]. Thus, in this study we investigated how carrageenan affects tumor cell cycle.. In this study we demonstrated cytotoxic effects of carrageenan towards cell cycle of human cancer cells in HeLa expressing FUCCI probes [24]. Two types of carrageenan, kappa (k-CO) and lambda (λ-CO) carrageenan were used because sulfate contents vary in each type of carrageenan [32]. These sulfated moieties in saccharides are believed to play an important role in manifestation of beneficial bioactivity [33]. Thus cytotoxic ...
Looking for online definition of Cell cycle regulatory protein in the Medical Dictionary? Cell cycle regulatory protein explanation free. What is Cell cycle regulatory protein? Meaning of Cell cycle regulatory protein medical term. What does Cell cycle regulatory protein mean?
See 13 Best Images of Cell Cycle And Mitosis Worksheet Answers. Inspiring Cell Cycle and Mitosis Worksheet Answers worksheet images. Cell Cycle Worksheet Answers Cell Cycle and Mitosis Worksheet Answer Key Cell Cycle Mitosis and Meiosis Test Answers Cell Cycle Worksheet Answer Key Cell Division Mitosis Worksheet and Answers Amyloid beta-peptide (Aβ), the neurotoxic component of senile plaques in Alzheimers disease (AD) brains, is known to trigger cell cycle reentry in post-mitotic neurons followed by apoptosis. However, the underlying mechanisms remain unclear. Recently, we have reported that Aβs stimulate the expression of inhibitor of differentiation-1 (Id1) to induce sonic hedgehog (SHH) (Hung et al., Mol Neurobiol 53(2):793-809, 2016), and both are mitogens capable of triggering cell cycle progression. In this work, we tested the hypothesis that Aβ-induced Id1 and SHH contribute to cell cycle reentry leading to apoptosis in neurons. We found that Aβ triggered cell cycle progression in the post-mitotic neurons, as indicated by the increased expression of two G1-phase markers including cyclin D1 and phosphorylated retinoblastoma protein (pRb), two G2-phase markers such as proliferating cell nuclear antigen (PCNA) and incorporation of 5-bromo-2′-deoxyuridine (BrdU) into newly synthesized ...
Cdc14 is an essential phosphatase in yeast but its role in the mammalian cell cycle remains obscure. We report here that Cdc14b-knockout cells display unscheduled induction of multiple cell cycle regulators resulting in early entry into DNA replication and mitosis from quiescence. Cdc14b dephosphorylates Ser5 at the C-terminal domain (CTD) of RNA polymerase II, a major substrate of cyclin-dependent kinases. Lack of Cdc14b results in increased CTD-Ser5 phosphorylation, epigenetic modifications that mark active chromatin, and transcriptional induction of cell cycle regulators. These data suggest a function for mammalian Cdc14 phosphatases in the control of transcription during the cell cycle ...
Second messengers control a wide range of important cellular functions in eukaryotes and prokaryotes. Here we show that cyclic di-GMP, a global bacterial second messenger, promotes cell cycle progression in Caulobacter crescentus by mediating the specific degradation of the replication initiation inhibitor CtrA. During the G1-to-S-phase transition, both CtrA and its cognate protease ClpXP dynamically localize to the old cell pole, where CtrA is rapidly degraded. Sequestration of CtrA to the cell pole depends on PopA, a newly identified cyclic di-GMP effector protein. PopA itself localizes to the cell pole and directs CtrA to this subcellular site via the direct interaction with a mediator protein, RcdA. We present evidence that c-di-GMP regulates CtrA degradation during the cell cycle by controlling the dynamic sequestration of the PopA recruitment factor to the cell pole. Furthermore, we show that cell cycle timing of CtrA degradation relies on converging pathways responsible for substrate and ...
Recent advances in defining the molecular mechanisms of cell cycle control in eukaryotes provide a basis for better understanding the hormonal control of cell proliferation in normal and neoplastic breast epithelium. It is now clear that a number of critical steps in cell cycle progression are controlled by families of serine/threonine kinases, the cdks. These kinases are activated by interactions with various cyclin gene products which form the regulatory subunits of the kinase complexes. Several families of cyclins control cell cycle progression in G1 phase, cyclins C, D and E, or in S, G2 and mitosis, cyclins A and B. Recent studies have defined the expression and regulation of cyclin genes in normal breast epithelial cells and in breast cancer cell lines. Following growth arrest of T-47D breast cancer cells by serum deprivation restimulation with insulin results in sequential induction of cyclin genes. Cyclin D1 mRNA increases within 1 h of mitogenic stimulation and is followed by increased
Bcl-2 protein has been contributed with number of genes which are involved in oncogenesis. Among the many targets of Bcl-2, NF kappa B have potential role in induction of cell cycle arrest. Curcumin has potential therapeutic effects against breast cancer through multiple signaling pathways. In this study, we investigated the role of curcumin in induction of cell cycle arrest via regulating of NF kappa B and polyamine biosynthesis in wt and Bcl-2+ MCF-7 cells. To examine the effect of curcumin on cell cycle regulatory proteins, PI3K/Akt, NF kappa B pathways and polyamine catabolism, we performed immunoblotting assay. In addition, cell cycle analysis was performed by flow cytometry. The results indicated that curcumin induced cell cycle arrest at G2/M phase by downregulation of cyclin B1 and Cdc2 and inhibited colony formation in MCF-7 wt cells. However, Bcl-2 overexpression prevented the inhibition of cell cycle associated proteins after curcumin treatment. The combination of LY294002, PI3K ...
Hematopoietic stem cells (HSCs) give rise to all blood populations due to their long-term self-renewal and multipotent differentiation capacities. Because they have to persist throughout an organisms life span, HSCs tightly regulate the balance between proliferation and quiescence. Here, we investigated the role of the transcription factor promyelocytic leukemia zinc finger (plzf) in HSC fate using the Zbtb16(lu/lu)mouse model, which harbors a natural spontaneous mutation that inactivates plzf. Regenerative stress revealed that Zbtb16(lu/lu)HSCs had a lineage-skewing potential from lymphopoiesis toward myelopoiesis, an increase in the long-term-HSC pool, and a decreased repopulation potential. Furthermore, oldplzf-mutant HSCs present an amplified aging phenotype, suggesting that plzf controls age-related pathway. We found that Zbtb16(lu/lu)HSCs harbor a transcriptional signature associated with a loss of stemness and cell cycle deregulation. Lastly, cell cycle analyses revealed an important ...
TY - JOUR. T1 - Cooperation between Different Forms of the Human Papillomavirus Type 1 E4 Protein To Block Cell Cycle Progression and Cellular DNA Synthesis. AU - Knight, G. L.. AU - Grainger, J. R.. AU - Gallimore, P. H.. AU - Roberts, S.. PY - 2004/12/15. Y1 - 2004/12/15. N2 - Posttranslational modification-oligomerization, phosphorylation, and proteolytic cleavage-of the human papillomavirus (HPV) E4 protein occurs as the infected keratinocytes migrate up through the suprabasal wart layers. It has been postulated that these events modify E4 function during the virus life cycle. In HPV type 1 (HPV1)-induced warts, N-terminal sequences are progressively cleaved from the full-length E4 protein (E1∧E4) of 17 kDa to produce a series of polypeptides of 16, 11 and 10 kDa. Here, we have shown that in human keratinocytes, a truncated protein (E4-16K), equivalent to the 16-kDa species, mediated a G2 arrest in the cell cycle that was dependent on a threonine amino acid in a proline-rich domain of the ...
Effects of treatment with serum-free medium and 25-hydroxycholesterol (25-OH) on the cell cycle of simian virus 40-transformed 3T3 fibroblasts, designated SV-3T3 cells, were studied and compared with simultaneous effects on the activity of 3-hydroxy-3-methylglutaryl (HMG) CoA reductase and incorporation of [3H]mevalonic acid into cholesterol, Coenzyme Q, and dolichol. The data confirm our previous finding (O. Larsson and A. Zetterberg, Cancer Res., 46: 1233-1239, 1986) that 25-OH inhibits the cell cycle traverse of SV-3T3 cells specifically in early G1. In contrast, treatment with serum-free medium had no effect on cell cycle progression. The effect of 25-OH on the cell cycle traverse was correlated to a substantial decrease in the activity of HMG CoA reductase, whereas there was no change in the rate of [3H]mevalonic acid incorporated into cholesterol, Coenzyme Q, and dolichol. When the cells were exposed to serum-free medium, there was no depression of activity of HMG CoA reductase, and the ...
Ribosome biogenesis and cell cycle are coordinated processes (Du and Stillman, 2001 Bernstein and Baserga, 2004; Fatica and Tollervey, 2002; Li et al., 2009; Strezoska et al., 2002). Mutations in genes encoding factors that are involved in ribosome biogenesis cause defects in ribosomal RNA processing as well as cell cycle arrest. Recent studies with mammalian cell lines have shown that ribosome biogenesis is also linked to tumorgenesis, that is mutation or depletion of ribosomal factors, leads to cancer cell proliferation (Montanaro et al., 2008). The yeast Saccharomyces cerevisiae is a useful model organism for understanding the connections between ribosome biogenesis and cell cycle control. Only a handful of studies have been done and these have mainly focused on different transacting factors involved in ribosome biogenesis; few studies have focused on the roles of r-proteins themselves in linking cell cycle progression and rRNA processing. I wanted to investigate what roles these r-proteins ...
Cell division is regulated by intricate and interconnected signal transduction pathways that precisely coordinate, in time and space, the complex series of events involved in replicating and segregating the component parts of the cell. In Trypanosoma brucei, considerable progress has been made over recent years in identifying molecular regulators of the cell cycle and elucidating their functions, although many regulators undoubtedly remain to be identified, and there is still a long way to go with respect to determining signal transduction pathways. However, it is clear that cell cycle regulation in T. brucei is unusual in many respects. Analyses of trypanosome orthologues of conserved eukaryotic cell cycle regulators have demonstrated divergence of their function in the parasite, and a number of other key regulators are missing from T. brucei. Cell cycle regulation differs in different parasite life cycle stages, and T. brucei appears to use different checkpoint control strategies compared to model
Since the frequencies of various erythroblast subpopulations were unchanged in DKO bone marrow (Figure 2A and B), we next investigated the erythroblast cell cycle. During terminal differentiation, erythroblasts undergo approximately 4-5 rapid cell divisions accompanied by a progressive decrease in cell size, followed by exit from the cell cycle.22 The decrease in erythroblast size during terminal maturation divisions has been attributed to the loss or alteration of the cell size control at the G1-S restriction point leading to the shortening of the G1 phase of the cell cycle without changes to the length of S and G2/M phase.23 To investigate changes in cell cycle time and G1 length in erythroblasts, we measured the length of various cell cycle phases in adult DKO mice bone marrow erythroblasts by cumulative BrdU labeling of bone marrow cells in culture (Figure 2H and I). The cell cycle time (Tc) and the length of S-phase (Ts) were calculated using the Nowakowski method.24 The cell cycle time for ...
Ribosomal protein L4 (RPL4) is a large ribosomal subunit protein that is structurally conserved in all kingdoms of life. This protein is a component of the 90S pre-ribosomal particle that initiates ribosomal assembly on the primary (35S) transcript. Here I show that in vivo repression of Rpl4p synthesis in S. cerevisiae results in severe loss of 60S ribosomal subunits and affects progression of the cell cycle. Analysis of rRNA processing suggests that these effects are associated with a block in the processing of the 27SA3 precursor RNA into 5.8S and 25S rRNA as well as a delay in processing of 35S precursor. More surprisingly, depletion of Rpl4p results in a unique bi-budded phenotype, with multiple cell cycle defects mainly affecting mitotic exit. To further characterize the role of RPL4 in cell cycle progression, I isolated temperature-sensitive L4 mutants. To date I have analyzed one of these mutants. Six hours after a temperature shift of this mutant, cells are uniformly arrested in SG2 ...
TY - JOUR. T1 - RAD9-dependent G1 arrest defines a second checkpoint for damaged DNA in the cell cycle of Saccharomyces cerevisiae. AU - Siede, Wolfram. AU - Friedberg, Andrew S.. AU - Friedberg, Errol C.. PY - 1993/9/1. Y1 - 1993/9/1. N2 - Exposure of the yeast Saccharomyces cerevisiae to ultraviolet (UV) light, the UV-mimetic chemical 4-nitroquinoline-1-oxide (4NQO), or γ radiation after release from G1 arrest induced by α factor results in delayed resumption of the cell cycle. As is the case with G2 arrest following ionizing radiation damage [Weinert, T. A. & Hartwell, L. H. (1988) Science 241, 317-322], the normal execution of DNA damage-induced G1 arrest depends on a functional yeast RAD9 gene. We suggest that the RAD9 gene product may interact with cellular components common to the G1/S and G2/M transition points in the cell cycle of this yeast. These observations define a checkpoint in the eukaryotic cell cycle that may facilitate the repair of lesions that are otherwise processed to ...
TY - JOUR. T1 - Clusterin and DNA repair. T2 - A new function in cancer for a key player in apoptosis and cell cycle control. AU - Shannan, B.. AU - Seifert, M.. AU - Boothman, D. A.. AU - Tilgen, W.. AU - Reichrath, J.. PY - 2006/9/1. Y1 - 2006/9/1. N2 - The glycoprotein clusterin (CLU), has two known isoforms generated in human cells. A nuclear form of CLU protein (nCLU) is pro-apoptotic, while a secretory form (sCLU) is pro-survival. Both forms are implicated in various cell functions, including DNA repair, cell cycle regulation, and apoptotic cell death. CLU expression has been associated with tumorigenesis and the progression of various malignancies. In response to DNA damage, cell survival can be enhanced by activation of DNA repair mechanisms, while simultaneously stimulating energy-expensive cell cycle checkpoints that delay the cell cycle progression to allow more time for DNA repair. This review summarizes our current understanding of the role of clusterin in DNA repair, apoptosis, and ...
Abstract: Prostate cancer remains a leading cause of death in men despite increased capacity to diagnose at earlier stages. After prostate cancer has become hormone independent which often occurs after hormonal ablation therapies it is difficult to effectively treat. Prostate cancer may arise from mutations and dysregulation of various genes involved in regulation signal transduction (e.g. PTEN Akt etc. ) and the cell cycle (e.g. p53 p21Cip1 p27Kip1 Rb etc. ). This review focuses on the aberrant interactions of signal transduction and cell cycle genes products and how they can contribute to prostate cancer and alter therapeutic effectiveness. Originally published Cell Cycle Vol. 7 No. 12 June 2008 ...
Single cell genomics and proteomics with the combination of innovative three-dimensional (3D) cell culture techniques can open new avenues toward the understanding of intra-tumor heterogeneity. Here, we characterize lung cancer markers using single cell mass cytometry to compare different in vitro cell culturing methods: two-dimensional (2D), carrier-free, or bead-based 3D culturing with in vivo xenografts. Proliferation, viability, and cell cycle phase distribution has been investigated. Gene expression analysis enabled the selection of markers that were overexpressed: TMEM45A, SLC16A3, CD66, SLC2A1, CA9, CD24, or repressed: EGFR either in vivo or in long-term 3D cultures. Additionally, TRA-1-60, pan-keratins, CD326, Galectin-3, and CD274, markers with known clinical significance have been investigated at single cell resolution. The described twelve markers convincingly highlighted a unique pattern reflecting intra-tumor heterogeneity of 3D samples and in vivo A549 lung cancer cells. In 3D systems CA9,
The mammalian BTG/Tob family is a group of proteins with anti-proliferative ability, and there are six members including BTG1, BTG2/PC3/Tis21, BTG3/ANA, BTG4/PC3B, Tob1/Tob and Tob2. Among them, Tob subfamily members, specifically Tob1/Tob and Tob2, have the most extensive C-terminal regions. As previously reported, overexpression of BTG/Tob proteins is associated with the inhibition of G1 to S-phase cell cycle progression and decreased cell proliferation in a variety of cell types. Tob subfamily proteins have similar anti-proliferative effects on cell cycle progression in cultured tumor cells. An important unresolved question is whether or not they have function in rapidly proliferating cells, such as embryonic stem cells (ESCs). Tob1 and Tob2 were expressed ubiquitously in mouse ESCs (mESCs), suggesting a possible role in early embryonic development and mESCs. To address the above question and explore the possible functions of the Tob subfamily in ESCs, we established ESCs from different ...
Biol. and in an affordable, high-throughput manner have constrained DNA damage and repair research on this topic. To resolve this, we developed an inexpensive, high capacity, 96-well plate-compatible alpha particle irradiator capable of delivering adjustable, low mGy/s particle radiation doses in multiple model systems Phthalylsulfacetamide and on the benchtop of a standard laboratory. The system enables Phthalylsulfacetamide monitoring alpha particle effects Phthalylsulfacetamide on DNA damage repair and signalling, genome stability pathways, oxidative stress, cell cycle phase distribution, cell viability and clonogenic survival using numerous microscopy-based and physical techniques. Most importantly, this method is foundational for high-throughput genetic screening and small molecule testing in mammalian and yeast cells. INTRODUCTION Since the discovery of radioactivity more than a century ago, science has made extraordinary progress on understanding the effects of ionizing radiation (IR) on ...
Stem cell self-renewal, commitment and reprogramming rely on a poorly understood coordination of cell cycle progression and execution of cell fate choices. Using existing experimental paradigms, it has not been possible to probe this relationship systematically in live stem cells in vitro or in vivo. Alterations in stem cell cycle kinetics probably occur long before changes in phenotypic markers are apparent and could be used as predictive parameters to reveal changes in stem cell fate. To explore this intriguing concept, we developed a single-cell tracking approach that enables automatic detection of cell cycle phases in live (stem) cells expressing fluorescent ubiquitylation-based cell-cycle indicator (FUCCI) probes. Using this tool, we have identified distinctive changes in lengths and fluorescence intensities of G1 (red fluorescence) and S/G2-M (green) that are associated with self-renewal and differentiation of single murine neural stem/progenitor cells (NSCs) and embryonic stem c
Synchronous cultures of Chlorella, that were obtained with minimum metabolic perturbation by centrifugal selection, reveal that progress through the cell cycle requires no change in the poly(A)+ mRNA population, although changes do occur during nutritional adaptation. Of the abundant soluble proteins, 93% are synthesized continuously through the cell cycle and those that are discontinuous show similar patterns in control cells. The synthesis of proteins is compared with parallel studies of accumulation of enzyme activity and it is shown that there is no discrepancy in their pattern of accumulation when both are studied under the same culture conditions. The eukaryote cell cycle can allow stable relative rates of synthesis of most proteins and balanced rates of accumulation of most enzyme activities. Macromolecule classes differ in their rates of accumulation throughout the cell cycle: total RNA increases linearly, poly(A)+ RNA accumulation is restricted to G1 phase, but total protein ...
TY - JOUR. T1 - Cell cycle dependent oscillatory expression of estrogen receptor-α links Pol II elongation to neoplastic transformation. AU - Vantaggiato, Cristina. AU - Tocchetti, Marta. AU - Cappelletti, Vera. AU - Gurtner, Aymone. AU - Villa, Alessandro. AU - Daidone, Maria Grazia. AU - Piaggio, Giulia. AU - Maggi, Adriana. AU - Ciana, Paolo. PY - 2014/7/1. Y1 - 2014/7/1. N2 - Decades of studies provided a detailed view of the mechanism of estrogen receptor-α (ERα) regulated gene transcription and the physio-pathological relevance of the genetic programs controlled by this receptor in a variety of tissues. However, still limited is our knowledge on the regulation of ERα synthesis. Preliminary observations showed that the expression of ERα is cell cycle regulated. Here, we have demonstrated that a well described polymorphic sequence in the first intron of ERα (PvuII and XbaI) has a key role in regulating the ERα content in cycling cells. We have shown that the RNA Pol II (Pol II) ...
In proliferating cells, the cell cycle consists of four phases. Gap 1 (G1) is the interval between mitosis and DNA replication that is characterized by cell growth. Replication of DNA occurs during the synthesis (S) phase, which is followed by a second gap phase (G2) during which growth and preparation for cell division occurs. Together, these three stages comprise the interphase phase of the cell cycle. Interphase is followed by the mitotic (M) phase. Mitosis and the production of two daughter cells occur in M phase. As the cell cycle controls cell replication and apoptosis, it is essential for the passage through the phases of the cell cycle and related processes to be regulated. Cyclin-dependent kinases (cdks), complexed with various cyclins, regulate the progression through G1-S-G2 phases by triggering DNA replication, transition from phase to phase, and transition into M phase. DNA synthesis occuring in the S phase is essential to passing on genetic information to daughter cells, but loss ...
Over a dozen of the leading scientific investigators in the cell cycle field will gather at the Salk including speakers from the University of Toronto, The Scripps Research Institute, The London Research Institute, The New York University School of Medicine, The Stowers Institute, Stanford University, Dana-Farber Cancer Institute, University of California Berkeley, The Ludwig Institute at UC San Diego, Edinburgh University, Ohio State University, Harvard University and The Sanford Burnham Institute. This symposium has become a labor of love and public service, said Dr. Tony Hunter, Professor, Molecular and Cell Biology Laboratory, Director of the Salk Institute Cancer Center and American Cancer Society Professor. Examining and sharing information about the crucial process of the cell cycle may lend new insights into the identification of biological markers that predict patients responsiveness to chemotherapy drugs and ultimately could lead to the development of new cancer drugs with fewer ...
Cells Alive Cell Cycle Worksheet 50 Cells Alive Worksheet Answer Key In 2020 one of Printable Worksheet Template - ideas, to explore this Cells Alive Cell Cycle Worksheet 50 Cells Alive Worksheet Answer Key In 2020 idea you can browse by and . We hope your happy with this Cells Alive Cell Cycle Worksheet 50 Cells Alive Worksheet Answer Key In 2020 idea. You can download and please share this Cells Alive Cell Cycle Worksheet 50 Cells Alive Worksheet Answer Key In 2020 ideas to your friends and family via your social media account. Back to 20 Cells Alive Cell Cycle Worksheet. ...
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BACKGROUND: Receptors belonging to the epidermal growth factor receptor (EGFR) family transfer extracellular signals by homotypic and heterotypic receptor interaction and cross-activation. Cell differentiation, death, and proliferation are regulated via these receptor-tyrosine-kinases. However, the initial mechanisms that lead to signal specificity and diversity, which cause a defined cellular response, are incompletely understood. We investigated the recruitment of receptor complexes in two c-erbB2-overexpressing breast carcinoma cell lines, SK-BR-3 and BT474, after ligand binding and its effects on intracellular signal transduction and cell cycle regulation. METHODS: In order to analyze the coaggregation of receptors on the cell surface induced by specific growth factor treatment, we used the flow cytometric Foerster-type fluorescence resonance energy transfer (FRET) technique. Cell cycle kinetics were monitored flow cytometrically via the anti-BrdU technique and acitivation of intracellular ...
TY - JOUR. T1 - Cell cycle analysis using flow cytometry. AU - Gray, J. W.. AU - Dolbeare, F.. AU - Pallavicini, M. G.. AU - Beisker, W.. AU - Waldman, F.. PY - 1986/1/1. Y1 - 1986/1/1. N2 - This manuscript reviews the utility of flow cytometry for the study of cell proliferation. The applications of univariate DNA distribution analysis to cytokinetic studies of asynchronous and perturbed cell populations are discussed briefly. The newly developed technique for simultaneous flow cytometric measurement of cellular DNA content and amount of incorporated bromodeoxyuridine is discussed in more detail. The cytochemistry required for this analysis is reviewed as are its applications to: (a) determination of the fractions of cells in the G1-, S- and G2 + M phases of the cell cycle; (b) determination of the G1-, S- and G2 + M phase durations and dispersions and growth fraction for asynchronous cells; (c) detection of ara-C resistant cells present at low frequency in an otherwise sensitive population; ...
TY - JOUR. T1 - The Aspergillus nidulans snt genes are required for the regulation of septum formation and cell cycle checkpoints. AU - Kraus, Peter R.. AU - Harris, Steven D.. PY - 2001/11/17. Y1 - 2001/11/17. N2 - In Aspergillus nidulans, germinating conidia undergo multiple rounds of nuclear division before forming a septum. Previous genetic results suggest that the ability to separate nuclear division and septum formation depends upon a threshold level of activity of the cyclin-dependent kinase NIMX,cdk1. Mutations in nimX and nimT, the gene encoding the NIMXcdk1-activating phosphatase, have revealed that Tyr-15 phosphorylation is important for determining the timing of the formation of the first septum. Here, we describe a screen for suppressors of nimT23 (snt), designed to identify additional components of the pathway regulating septum formation. We show that a subset of the snt mutants are defective in the temporal regulation of septum formation and in cell cycle checkpoint responses. ...
Nitrogen Cycle Process Essay. Essay on the Nitrogen Cycle - Biology Discussion on the nitrogen cycle. Nitrogen is one of In nitrogen cycle, free N2 gas of atmosphere is converted into ammonia or oxidised to nitrate at different stages. Blue green algae In this process nitrogen in organic matter of dead plants and animals is converted to ammonia and amino acids. Urea is applied in nbsp; The Nitrogen Cycle is the Most Important Biogeochemical Cycle about The Process of Nitrogen Cycle - The environment is stabilized by the biogeochemical cycles. Biogeochemical cycles are the processes that occur naturally and recycle the nutrients in different chemical forms from the non-living ecosystem to living organisms and then back to the non-living ecosystem. Free nitrogen cycle Essays and Papers - of Nitrogen Cycle - The environment is stabilized by the biogeochemical cycles. Biogeochemical cycles are the processes that occur naturally and recycle the nutrients in different chemical forms from the ...
TY - JOUR. T1 - Cell-cycle-based strategies to drive myocardial repair. AU - Zhu, Wuqiang. AU - Hassink, Rutger J.. AU - Rubart, Michael. AU - Field, Loren J.. N1 - Copyright: Copyright 2009 Elsevier B.V., All rights reserved.. PY - 2009/7. Y1 - 2009/7. N2 - Cardiomyocytes exhibit robust proliferative activity during development. After birth, cardiomyocyte proliferation is markedly reduced. Consequently, regenerative growth in the postnatal heart via cardiomyocyte proliferation (and, by inference, proliferation of stem-cell-derived cardiomyocytes) is limited and often insufficient to affect repair following injury. Here, we review studies wherein cardiomyocyte cell cycle proliferation was induced via targeted expression of cyclin D2 in postnatal hearts. Cyclin D2 expression resulted in a greater than 500-fold increase in cell cycle activity in transgenic mice as compared to their nontransgenic siblings. Induced cell cycle activity resulted in infarct regression and concomitant improvement in ...
The aim of the present work was to investigate the occurrence of the cell cycle during germination as related to thermodormancy in barley (Hordeum vulgare L., cv. Pewter) grains in relation with abscisic acid (ABA) by: (i) flow cytometry to determine the progression of the cell cycle; and (ii) reverse transcription-PCR to characterize the expression of some important genes involved in cell-cycle regulation. In dry embryos, cells are mostly (82%) arrested in G1 phase of the cell cycle, the remaining cells being in the G2 (17%) or S phase (0.9%). Germination at 20 °C was associated with an increase in the nuclei population in G2 and S (up to 32.5-44.5 and 9.2-11.3%, respectively, after 18-24h). At 30 °C, partial reactivation of the cell cycle occurred in embryos of dormant grains that did not germinate. Incubation with 50mM hydroxyurea suggests that thermodormancy resulted in a blocking of the nuclei in the S phase. In dry dormant grains, transcripts of CDKA1, CYCA3, KRP4, and WEE1 were present, while
Author Summary Cellular and viral life cycles are connected through multiple, though poorly understood, mechanisms. Parvoviruses infect humans and a broad spectrum of animals, causing a variety of diseases, but they are also used in experimental cancer therapy and serve as vectors for gene therapy. Parvoviruses can only multiply in proliferating cells providing essential replicative and transcriptional functions. However, it is unknown whether the cell cycle regulatory machinery may also control parvovirus assembly. We found that the nuclear translocation of parvovirus MVM capsid subunits (VPs) was highly dependent on physiological cell cycle regulations in mammalian fibroblasts, including: quiescence, progression through G1/S boundary, DNA synthesis, and cell to cell contacts. VPs nuclear translocation was significantly more sensitive to cell cycle controls than viral genome replication and gene expression. The results support nuclear capsid assembly as the major driving process of parvoviruses
"SON Controls Cell-Cycle Progression by Coordinated Regulation of RNA Splicing". Molecular Cell. 42 (2): 185-198. doi:10.1016/j. ... "Son Is Essential for Nuclear Speckle Organization and Cell Cycle Progression". Molecular Biology of the Cell. 21 (4): 650-663. ... SON-dependent cell-cycle genes possess a weak 5' or 3' splice site and are dependent on SON to ensure efficient splicing and ... The SON gene is required for RNA splicing of transcripts encoding the cell-cycle protein TUBG1 and genes maintaining hESC ...
Cell Cycle. 6 (6): 750-7. doi:10.4161/cc.6.6.3986. PMC 2040307. PMID 17361101. Lin Q, Yang W, Baird D, Feng Q, Cerione RA ( ... Côté JF, Vuori K (August 2007). "GEF what? Dock180 and related proteins help Rac to polarize cells in new ways". Trends in Cell ... endocytosis and cell cycle progression. Gene expression studies have suggested that Dock11 may have a role in the development ... Meller N, Merlot S, Guda C (November 2005). "CZH proteins: a new family of Rho-GEFs". Journal of Cell Science. 118 (Pt 21): ...
... is a protein that slows cell division by slowing the progression of the cell cycle from the G1 phase to the S phase, thereby ... p16 is an inhibitor of cyclin-dependent kinases (CDK). It slows down the cell cycle by prohibiting progression from G1 phase to ... Ivanchuk SM, Mondal S, Rutka JT (June 2008). "p14ARF interacts with DAXX: effects on HDM2 and p53". Cell Cycle. 7 (12): 1836-50 ... Serrano M, Hannon GJ, Beach D (December 1993). "A new regulatory motif in cell-cycle control causing specific inhibition of ...
Cell Cycle. 8 (24): 4127-4137. doi:10.4161/cc.8.24.10240. PMID 19946211. Song, Byeongwoon; Young, C. S. H. (April 1998). " ... and immunity in various cells, but specifically hepatocytes, adipocytes, and hematopoietic cells. For example, in adipocytes, ... And furthermore, in cells lacking C/EBP or in C/EBP-deficient mice, both are unable to undergo adipogenesis. This results in ... It is frequently absent from genes that encode proteins used in virtually all cells. This box along with the GC box is known ...
Cell Cycle. 8 (17): 2756-68. doi:10.4161/cc.8.17.9387. PMID 19652553. Bianchi N, Zuccato C, Lampronti I, Borgatti M, Gambari R ... "MicroRNA-210 regulates mitochondrial free radical response to hypoxia and krebs cycle in cancer cells by targeting iron sulfur ... Cell. 35 (6): 856-67. doi:10.1016/j.molcel.2009.09.006. PMC 2782615. PMID 19782034. Chan SY, Zhang YY, Hemann C, Mahoney CE, ... Cell Metab. 10 (4): 273-84. doi:10.1016/j.cmet.2009.08.015. PMC 2759401. PMID 19808020. Bostjancic E, Zidar N, Glavac D (2009 ...
Peter ME (2009). "Let-7 and miR-200 microRNAs: guardians against pluripotency and cancer progression". Cell Cycle. 8 (6): 843- ... 4T1 cells) but not in other cells which are unable to colonize (4TO7 cells). Overexpression of miR-200c in non-metastatic 4TO7 ... In a series of mouse mammary isogenic cancer cell lines, the miR-200 family is highly expressed only in the cells that are able ... While the mir-200 family is highly expressed in normal epithelial cells, it is not expressed in normal fibroblast cells that ...
Macy B, Wang M, Yu HG (2009). "The many faces of shugoshin, the "guardian spirit," in chromosome segregation". Cell Cycle. 8 (1 ... It senses tension between sister chromatids during mitosis, and it degrades when they separate preventing cell cycle arrest and ... Cell Cycle. 5 (10): 1094-101. doi:10.4161/cc.5.10.2747. PMID 16687935. Salic A, Waters JC, Mitchison TJ (2004). "Vertebrate ... doi:10.1016/j.cell.2004.08.016. PMID 15339662. S2CID 14339817. Xu Z, Cetin B, Anger M, Cho US, Helmhart W, Nasmyth K, et al. ( ...
January 2006). "R-Spondin proteins: a novel link to beta-catenin activation". Cell Cycle. 5 (1): 23-6. doi:10.4161/cc.5.1.2305 ... Developmental Cell. 7 (4): 525-34. doi:10.1016/j.devcel.2004.07.019. PMID 15469841. Jin YR, Turcotte TJ, Crocker AL, Han XH, ...
Cell Cycle. 16 (14): 1345-1349. doi:10.1080/15384101.2017.1334022. PMC 5539816. PMID 28657421. Barranco Quintana, JL; Allam, MF ... It is currently unclear why brain volume decreases with age, however, a few causes may include: cell death, decreased cell ... Treatments with anticancer chemotherapeutic agents often are toxic to the cells of the brain, leading to memory loss and ...
Cell Cycle. 14 (14): 2226-2250. doi:10.1080/15384101.2015.1053672. PMC 4615001. PMID 26030272. Robles P, Quesada V (December ... Cell Cycle. 14 (14): 2226-2250. doi:10.1080/15384101.2015.1053672. PMC 4615001. PMID 26030272. Robles P, Quesada V (December ... Cell Systems. 2 (2): 101-111. doi:10.1016/j.cels.2016.01.013. PMID 27135164. Hamers L (2016). "Why do our cell's power plants ... Encyclopedia of Cell Biology. Waltham: Academic Press. pp. 545-554. doi:10.1016/b978-0-12-394447-4.10066-5. ISBN 978-0-12- ...
"MicroRNA-221-222 regulate the cell cycle in mast cells". Journal of Immunology. 182 (1): 433-445. doi:10.4049/jimmunol.182.1. ... Sun T, Yang M, Kantoff P, Lee GS (2009). "Role of microRNA-221/-222 in cancer development and progression". Cell Cycle. 8 (15 ... It targets CD117, which then prevents cell migration and proliferation in endothelial cells. miR-221 is known as an anti ... and MEK/ERK-mediated cell cycle regulation". Biol Chem. 391 (7): 791-801. doi:10.1515/BC.2010.072. PMID 20624000. S2CID ...
Cell Cycle. 8 (21): 3469-73. doi:10.4161/cc.8.21.9837. PMC 3593963. PMID 19829088. Zeng L, Carter AD, Childs SJ (Oct 2009). " ... and KLF4 and represses pluripotency in human embryonic stem cells". Cell. 137 (4): 647-58. doi:10.1016/j.cell.2009.02.038. PMID ... Chivukula RR, Mendell JT (May 2009). "Abate and switch: miR-145 in stem cell differentiation". Cell. 137 (4): 606-8. doi: ... independent cell death in urothelial cancer cell lines with targeting of an expression signature present in Ta bladder tumors ...
Cell Cycle. 5 (13): 1407-10. doi:10.4161/cc.5.13.2924. PMID 16855396. Gururaj AE, Peng S, Vadlamudi RK, Kumar R (2007). " ... BCAS3 is a gene that is amplified and overexpressed in breast cancer cells. The BCAS3 gene is regulated by estrogen receptor ...
Cell Cycle. 6 (6): 643-6. doi:10.4161/cc.6.6.4033. PMID 17374991. Shi Y, Zou M, Farid NR, Paterson MC (December 2000). " ... Cell. 84 (4): 587-97. doi:10.1016/S0092-8674(00)81034-X. PMID 8598045. S2CID 18792069. Pekarsky Y, Campiglio M, Siprashvili Z, ...
Azzalin CM, Lingner J (2006). "The double life of UPF1 in RNA and DNA stability pathways". Cell Cycle. 5 (14): 1496-8. doi: ... Cell. 12 (3): 675-87. doi:10.1016/S1097-2765(03)00349-6. PMID 14527413. Yamashita A, Ohnishi T, Kashima I, Taya Y, Ohno S (2001 ... Cell. Biol. 21 (1): 209-23. doi:10.1128/MCB.21.1.209-223.2001. PMC 88795. PMID 11113196. Lykke-Andersen J, Shu MD, Steitz JA ( ... Cell. Biol. 20 (23): 8944-57. doi:10.1128/MCB.20.23.8944-8957.2000. PMC 86549. PMID 11073994. Serin G, Gersappe A, Black JD, et ...
Cell Cycle. 2004 Dec;3(12):1612-37. doi: 10.4161/cc.3.12.1345. Epub 2004 Dec 20. PMID 15611647 Bernstein H, Bernstein C. Sexual ... Cellular compartments in cell biology comprise all of the closed parts within the cytosol of a eukaryotic cell, usually ... The eukaryotic cell is thought to have arisen when an ancestral archaeal cell internalized an aerobic bacterium (the proto- ... It was thought that compartmentalization is not found in prokaryotic cells., but the discovery of carboxysomes and many other ...
"ING4 induces G2/M cell cycle arrest and enhances the chemosensitivity to DNA-damage agents in HepG2 cells". FEBS Letters. 570 ( ... Cell Cycle. 4 (9): 1153-6. doi:10.4161/cc.4.9.2040. PMID 16096374. Bonaldo MF, Lennon G, Soares MB (September 1996). " ... The protein encoded by this gene is similar to ING1, a tumor suppressor protein that can interact with TP53, inhibit cell ... Molecular Cell. 23 (4): 607-18. doi:10.1016/j.molcel.2006.06.026. PMID 16916647. Unoki M, Shen JC, Zheng ZM, Harris CC ( ...
2007). "Replication stress, defective S-phase checkpoint and increased death in Plk2-deficient human cancer cells". Cell Cycle ... Ma S, Charron J, Erikson RL (2003). "Role of Plk2 (Snk) in mouse development and cell proliferation". Mol. Cell. Biol. 23 (19 ... Serum-inducible kinase is a member of the 'polo' family of serine/threonine protein kinases that have a role in normal cell ... 2003). "Silencing of the novel p53 target gene Snk/Plk2 leads to mitotic catastrophe in paclitaxel (taxol)-exposed cells". Mol ...
Cell division cycle protein 27 homolog is a protein that in humans is encoded by the CDC27 gene. The protein encoded by this ... "Entrez Gene: CDC27 cell division cycle 27 homolog (S. cerevisiae)". Vodermaier HC, Gieffers C, Maurer-Stroh S, Eisenhaber F, ... Overview of all the structural information available in the PDB for UniProt: P30260 (Cell division cycle protein 27 homolog) at ... Cell Cycle. 1 (4): 282-92. doi:10.4161/cc.1.4.139. PMID 12429948. Human CDC27 genome location and CDC27 gene details page in ...
Cell Cycle. 8 (5): 677-8. doi:10.4161/cc.8.5.8065. PMC 2710531. PMID 19223763. Antunica-Noguerol, M; Budziñski, M L; Druker, J ... Cell. 131 (2): 309-23. doi:10.1016/j.cell.2007.07.044. hdl:20.500.12110/paper_00928674_v131_n2_p309_CarbiaNagashima. PMID ... January 1993). "Interleukin involvement in anterior pituitary cell growth regulation: effects of IL-2 and IL-6". Endocrinology ... January 2006). "Bone morphogenetic protein-4 inhibits corticotroph tumor cells: involvement in the retinoic acid inhibitory ...
2008). "Direct role of nucleotide metabolism in C-MYC-dependent proliferation of melanoma cells". Cell Cycle. 7 (15): 2392-400 ... 2006). "A protein-protein interaction network for human inherited ataxias and disorders of Purkinje cell degeneration". Cell. ... doi:10.1016/j.cell.2006.03.032. PMID 16713569. S2CID 13709685. He Y, Mou Z, Li W, et al. (2009). "Identification of IMPDH2 as a ... Cell Genet. 82 (3-4): 145-6. doi:10.1159/000015088. PMID 9858805. S2CID 46764436. Pua KH, Stiles DT, Sowa ME, Verdine GL (10 ...
Cell Cycle. 5 (1): 23-26. doi:10.4161/cc.5.1.2305. PMID 16357527. Seitz, C. S.; Van Steensel, M.; Frank, J.; Senderek, J.; ...
Cell Cycle. 3 (6): 823-8. doi:10.4161/cc.3.6.938. PMID 15197343. Kohane, I. S.; Masys, D. R.; Altman, R. B. (2006). "The ... The process of tumorigenesis that transforms a normal cell to a cancerous cell involve a series of complex genetic and ... February 2007). "The Epigenomics of Cancer". Cell. 128 (4): 683-92. doi:10.1016/j.cell.2007.01.029. PMC 3894624. PMID 17320506 ... If cell survival is determined by many mutations of small effect, it is unlikely that genome sequencing will uncover a single " ...
Wan Y, Chang HY (September 2010). "HOTAIR: Flight of noncoding RNAs in cancer metastasis". Cell Cycle. 9 (17): 3391-2. doi: ... Woo CJ, Kingston RE (June 2007). "HOTAIR lifts noncoding RNAs to new levels". Cell. 129 (7): 1257-9. doi:10.1016/j.cell.2007.06 ... "Phosphorylation of the PRC2 component Ezh2 is cell cycle-regulated and up-regulates its binding to ncRNA". Genes & Development ... doi:10.1016/j.cell.2007.05.022. PMC 2084369. PMID 17604720. Tsai MC, Manor O, Wan Y, Mosammaparast N, Wang JK, Lan F, et al. ( ...
Cowling, Victoria H.; Cole, Michael D. (15 April 2007). "HATs Off to Capping: A New Mechanism for Myc". Cell Cycle. 6 (8): 907- ... "Women in Cell Biology Early Career Medal Winner: Victoria Cowling , British Society for Cell Biology". Retrieved 24 January ... In 2014, Cowling was awarded the Women in Cell Biology Early Career Medal from the British Society for Cell Biology. In 2014, ... In 2017, Cowling was awarded an ERC consolidator grant to investigate mRNA cap regulation and function in CD8 T cells. In 2018 ...
Cell Cycle. 8 (6): 952-954. doi:10.4161/cc.8.6.7905. PMID 19221499. Cayrol B, Geinguenaud F, Lacoste J, et al. (2009). "Auto- ...
Overexpression of miR-26a brings about negative regulation of both cell proliferation and of the cell cycle. Therapeutic miR- ... which in turn causes inhibition of cell growth and cell-cycle progression. miR-26a again suppresses tumorigenesis in ... cell line LoVo cells, compared with other three colorectal cell lines SW480, HT29 and Caco-2. Overexpression of miR-26b ... "Human embryonic stem cells and metastatic colorectal cancer cells shared the common endogenous human microRNA-26b". J Cell Mol ...
"HIV1 Vpr arrests the cell cycle by recruiting DCAF1/VprBP, a receptor of the Cul4-DDB1 ubiquitin ligase". Cell Cycle. 6 (2): ... Wen X, Duus KM, Friedrich TD, de Noronha CM (September 2007). "The HIV1 protein Vpr acts to promote G2 cell cycle arrest by ... E3 ubiquitin ligase to modulate cell cycle". Proceedings of the National Academy of Sciences of the United States of America. ... "Targeted Vpr-derived peptides reach mitochondria to induce apoptosis of alphaVbeta3-expressing endothelial cells". Cell Death ...
Malicet C, Dagorn JC, Neira JL, Iovanna JL (2006). "p8 and prothymosin alpha: unity is strength". Cell Cycle. 5 (8): 829-30. ... 2006). "Cell growth-dependent subcellular localization of p8". J. Cell. Biochem. 97 (5): 1066-79. doi:10.1002/jcb.20682. PMID ... 2007). "The SYT-SSX fusion protein down-regulates the cell proliferation regulator COM1 in t(x;18) synovial sarcoma". Mol. Cell ... Cell. Biol. 27 (3): 993-1006. doi:10.1128/MCB.00996-06. PMC 1800682. PMID 17116693. v t e (Articles with short description, ...
... including 3 members of a family related to the cell cycle regulator nimA of Aspergillus nidulans". Cell Growth & ... Cell Cycle. 14 (2): 189-199. doi:10.4161/15384101.2014.973743. PMC 4353221. PMID 25607644. Romano D, Matallanas D, Weitsman G, ... Cell. 127 (3): 635-48. doi:10.1016/j.cell.2006.09.026. PMID 17081983. S2CID 7827573. Seidel C, Schagdarsurengin U, Blümke K, ... Research has shown that in cells with loss of PTEN (gene), a tumor suppressor that is frequently mutated in cancers, Akt ...
Leydig cell tumors of the testis and pancreatic acinar cell tumors and dietary PFOA consumption.[40] The C8 Science Panel ... "PFAS 'forever chemicals' constantly cycle through ground, air and water, study finds". The Guardian ... between elevated C8 exposure and liver adenomas or pancreatic acinar cell tumors; however, a probable link[vague] was found ... cell infiltration of the placenta to facilitate trophoblastic integration with placental blood supply.[45] Another mechanism ...
"Cell. 126 (1): 107-120. doi:10.1016/j.cell.2006.05.036. PMID 16839880. S2CID 15006256.. ... The resulting acetyl-CoA enters the citric acid cycle (or Krebs Cycle), where the acetyl group of the acetyl-CoA is converted ... All cells contain the enzyme hexokinase, which catalyzes the conversion of glucose that has entered the cell into glucose-6- ... Hexokinase is inhibited by high levels of G6P in the cell. Thus the rate of entry of glucose into cells partially depends on ...
"UNEP and Daimler Call for Infrastructure for Electric and Fuel-cell Vehicles". 4 July 2008. Archived from the ...
These are found in all cell membranes and the membranes of most cell organelles.[2] Phosphatidylcholines are structurally ... "Dietary Choline Intake: Current State of Knowledge Across the Life Cycle". Nutrients. 10 (10): 1513. doi:10.3390/nu10101513 ... Choline is stored in the cell membranes and organelles as phospholipids, and inside cells as phosphatidylcholines and ... Acetylcholine is even present in the placenta and may help control cell proliferation and differentiation (increases in cell ...
Many neuronal cells are unresponsive to stimulation by IL-6 alone, but differentiation and survival of neuronal cells can be ... leading to a cycle of inhibition and disinhibition.[78] These neural oscillations are impaired in schizophrenia, and these ... It supports the growth of B cells and is antagonistic to regulatory T cells. ... production of breast cancer stem cell-like cells,[68] metastasis through down-regulation of E-cadherin,[69] and alteration of ...
"Life-like cells are made of metal". New Scientist. September 14, 2011. Retrieved 2014-05-25.. ... Many Earth plants and animals undergo major biochemical changes during their life cycles as a response to changing ... A hypothetical cell membrane termed an azotosome, capable of functioning in liquid methane in Titan conditions was computer- ... The Cronin group at Glasgow University reported self-assembly of tungsten polyoxometalates into cell-like spheres.[27] By ...
... above but depends critically on the existence of an excitation anode to maintain an arc discharge during the half-cycle when ... Memory cell. *Mixed-signal integrated circuit. *MOS integrated circuit (MOS IC). *Organic semiconductor ...
... cell type, cell cycle stage, external factors, presence of other binding proteins, etc. - as it happens with most of the ... One example of a manually produced molecular interaction map is the Kurt Kohn's 1999 map of cell cycle control.[68] Drawing on ... Cell Biol. Advances in Molecular and Cell Biology. Vol. 14. pp. 29-55. doi:10.1016/S1569-2558(08)60339-2. ISBN 9780762301133. . ... The activity of the cell is regulated by extracellular signals. Signal propagation inside and/or along the interior of cells ...
A position was transcribed by cycling through the pieces in a position, indexing the corresponding random numbers (vacant ... and the hashing function can be interpreted as a partition of that space into a grid of cells. The table is often an array with ...
In biology, polymorphism[1] is the occurrence of two or more clearly different morphs or forms, also referred to as alternative phenotypes, in the population of a species. To be classified as such, morphs must occupy the same habitat at the same time and belong to a panmictic population (one with random mating).[2] Put simply, polymorphism is when there are two or more possibilities of a trait on a gene. For example, there is more than one possible trait in terms of a jaguar's skin colouring; they can be light morph or dark morph. Due to having more than one possible variation for this gene, it is termed 'polymorphism'. However, if the jaguar has only one possible trait for that gene, it would be termed "monomorphic". For example, if there was only one possible skin colour that a jaguar could have, it would be termed monomorphic. The term polyphenism can be used to clarify that the different forms arise from the same genotype. Genetic polymorphism is a term used somewhat differently by ...
Cell》 89: 263-73. PMID 9108481. 2009년 3월 31일에 확인함.. CS1 관리 - 여러 이름 (링크) ... Watch an animated tutorial on the life cycle of HIV Archived 2006년 6월 16일 - 웨이백 머신 ... Clapham PR, McKnight A. (2001). "HIV-1 receptors and cell tropism". 》Br Med Bull.》 58 (4): 43-59. doi:10.1093/bmb/58.1.43. PMID ... Garcia JV, Miller AD (1991년 4월). "Serine phosphorylation-independent downregulation of cell-surface CD4 by nef". 》Nature》 350 ( ...
"Ammonia for fuel cells". Retrieved 5 September 2019.. *^ "Survey reveals aluminum remains fastest growing automotive ... cycling, and walking. Bicycle sharing systems have been established in China and many European cities, including Copenhagen and ... Research into alternative forms of power includes using ammonia instead of hydrogen in fuel cells.[93] ...
Cell phone reception can be sporadic and, when available, signal strength and clarity is poor. Although the surrounding ... Cycling on Angeles Crest Highway. *Caltrans: Current road conditions and closures on Angeles Crest Highway ...
Cell Cycle 8 (24): 4155-67։ December 2009։ PMC 2896895։ PMID 19946220։ doi:10.4161/cc.8.24.10316 CS1 maint: display-authors ( ... 74,0 74,1 «Small-cell carcinoma of the prostate»։ Journal of the Royal Society of Medicine 90 (6): 340-1։ June 1997։ PMC ... 75,0 75,1 «[Clinicopathological characterization of prostatic small cell carcinoma: a case report and review of the literature ... Expression of prostate-specific membrane antigen (PSMA), increases cell folate uptake and proliferation and suggests a novel ...
Life cycle[edit]. Settlement and early life stages of scleractinian corals. This figure highlights on the first steps of a ... There are sometimes as many as five million cells of these per 1 square centimetre (0.16 sq in) of coral tissue. Up to 50% of ... Stony corals are closely related to sea anemones, and like them are armed with stinging cells known as cnidocytes. Corals ... In reef-forming corals, the endodermal cells are usually replete with symbiotic unicellular dinoflagellates known as ...
Electroporation allows the cell membrane to open up after applying an electric field. By applying short, high voltage pulses to ... Similarly, the gas bubble will dramatically decay in size when encountering the other positive half of the pressure cycle.[1] ... Since there exists a need to enhance gene transfer into cells, sonophoresis has the ability to achieve higher transfection rate ... Stable cavitation is when cavitation bubbles persist over many acoustic pressure cycles without collapsing. On the other hand, ...
"Biological products include a wide range of products such as vaccines, blood and blood components, allergenics, somatic cells, ... A systematic review of drug life cycles, therapeutic drug markets and regulatory frameworks". PLOS ONE. 12 (8): e0182613. ... "drugs derived from living cells"[7] that are injectable or infused (although some are oral medications).[4] They are used to ... "drugs derived from living cells"-but biologics are "not always deemed to be specialty drugs".[7] Biologics "may be produced by ...
In addition to the distribution of almost the whole Psalter over a four-week cycle, the Church also provides appropriate hymns ... but the cycle of prayer became the norm in daily life in monasteries. By the fourth century, the characteristics of the ... and it provides the Benedictus and Magnificat on each Sunday with three antiphons that reflect the three-year cycle of Gospel ... for the new saints added to the General Roman Calendar as well as the Benedictus and Magnificat antiphons for the 3-year cycle ...
... by means of beta-oxidation followed by further combustion in the citric acid cycle to CO2 and water. Cells in the central ... They can be taken up from the blood by all cells that have mitochondria (with the exception of the cells of the central nervous ... Studies on the cell membranes of mammals and reptiles discovered that mammalian cell membranes are composed of a higher ... the cell wall, and the membranes that enclose all the organelles within the cells, such as the nucleus, the mitochondria, ...
... which can help in the interpretation of their life cycle, living interactions, natural environment, communities, and manner of ...
"Id2 specifically alters regulation of the cell cycle by tumor suppressor proteins"، Mol. Cell. Biol.، 16 (6): 2570-8، 1996، PMC ... negative regulation of neural precursor cell proliferation. • neuron differentiation. • regulation of cell cycle. ... positive regulation of transcription involved in G1/S transition of mitotic cell cycle. • نمو متعدد الخلايا. • ‏GO:0045996 ... regulation of G1/S transition of mitotic cell cycle. • rhythmic process. • negative regulation of DNA-binding transcription ...
Glycogen is found in the form of granules in the cytosol in many cell types, and plays an important role in the glucose cycle. ... Glycogen is a polysaccharide that is the principal storage form of glucose in animal cells. ...
... s are also used in the cells of organisms in a process known as cellular respiration, where organic molecules are oxidized ... which can combine to form helium through the proton-proton chain reaction or by the CNO cycle. When the hydrogen fuel is ... and ultimately disposing of nuclear fuel together make up the nuclear fuel cycle. Not all types of nuclear fuels create power ...
The early 6th-century Dashavatara Temple in the Deogarh complex has a simple, one-cell plan. ... recombine and recreate the cycle of life. Small temples were often dedicated to Shiva and his family (wife Durga, son Ganesha ... and the cell (pinda) by a unique plan based on astronomical numbers.[22] Subhash Kak sees the temple form and its iconography ... cell) structure to large nearby complexes. These stepwells and their temple compounds have been variously dated from late 1st ...
"Carbon Cycle". NASA. Archived from the original on 2013-03-02. Retrieved 2009-06-24.. ... "Expansion of the Hadley cell under global warming" (PDF). Geophysical Research Letters. 34: L06805. doi:10.1029/2006GL028443 ... "The Carbon Cycle and Atmospheric Carbon Dioxide: SRES scenarios and their implications for future CO2 concentration". Climate ... "Atmospheric brown clouds: Impacts on South Asian climate and hydrological cycle". Proc. Natl. Acad. Sci. 102 (15): 5326-5333. ...
Evolutionary psychology has proposed several explanations for love. Monkey infants and children are for a very long time dependent on parental help. Love has therefore been seen as a mechanism to promote mutual parental support of children for an extended time period. Another is that sexually transmitted diseases may cause, among other effects, permanently reduced fertility, injury to the fetus, and increase risks during childbirth. This would favor exclusive long-term relationships reducing the risk of contracting an STD.[1] From the perspective of evolutionary psychology the experiences and behaviors associated with love can be investigated in terms of how they have been shaped by human evolution.[2] For example, it has been suggested that human language has been selected during evolution as a type of "mating signal" that allows potential mates to judge reproductive fitness.[3] Miller described evolutionary psychology as a starting place for further research: "Cognitive neuroscience could try ...
The Prose Lancelot or Vulgate Cycle includes passages from that period. This collection indirectly led to Thomas Malory's Le ... See also: Cell phone novel, Visual novel, Hypertext fiction, and Interactive fiction ... the North Germanic Edda and the Arthurian Cycles. ...
Eukaryotic cells respond to damaged DNA by stimulating or impairing G1, S, or G2 phases of the cell cycle to initiate DNA ... the cycle progresses compared to an average cycle. - The ranges denoted Inter-cycle variability are more appropriate to use in ... Estradiol is produced by action of aromatase mainly in the Leydig cells of the mammalian testis, but also by some germ cells ... Estradiol levels across the menstrual cycle in 36 normally cycling, ovulatory women, based on 956 specimens.[60] The horizontal ...
If one were to plot the electric field vector over one cycle of oscillation, an ellipse would generally be obtained, as is ... However, when a voltage is applied across a cell, the molecules straighten out, lessening or totally losing the circular ... The first two diagrams below trace the electric field vector over a complete cycle for linear polarization at two different ... where angular brackets denote averaging over many wave cycles. Several variants of the coherency matrix have been proposed: the ...
Cohen BA, Colas P, Brent R (Nov 1998). „An artificial cell-cycle inhibitor isolated from a combinatorial library". Proc Natl ...
Controlling the Cell Cycle The cell cycle & Cell death Transcriptional program of the cell cycle: high-resolution timing Cell ... Cell cycle checkpoints are used by the cell to monitor and regulate the progress of the cell cycle. Checkpoints prevent cell ... This cyclin-Cdk driven cell cycle transitional mechanism governs a cell committed to the cell cycle that allows cell ... Using GFP to visualize the cell-cycle Science Creative Quarterlys overview of the cell cycle KEGG - Human Cell Cycle Archived ...
cell division cycle 73 Paf1/RNA polymerase II complex component-like protein. cell division cycle 73, Paf1/RNA polymerase II ... Cell-cell adhesion regulates Merlin/NF2 interaction with the PAF complex. Title: Cell-cell adhesion regulates Merlin/NF2 ... cell division cycle 73provided by HGNC. Primary source. HGNC:HGNC:16783 See related. Ensembl:ENSG00000134371 MIM:607393; ... involved_in negative regulation of G1/S transition of mitotic cell cycle IDA Inferred from Direct Assay. more info ...
Its dysregulation has devastating consequences, including cancer,sup,1-3,/sup,. The cell cycle is driven by precise regulation ... over which cells grow and divide, is a fundamental process of life. ... Our results show that cell cycle progression explains less than half of all cell-to-cell variability, and that most cycling ... Spatiotemporal dissection of the cell cycle with single-cell proteogenomics Nature. 2021 Feb;590(7847):649-654. doi: 10.1038/ ...
Progression through the phases of the mitotic cell cycle, the most common eukaryotic cell cycle, which canonically comprises ... In some variant cell cycles nuclear replication or nuclear division may not be followed by cell division, or G1 and G2 phases ... Gene Ontology Term: mitotic cell cycle. GO ID. GO:0000278 Aspect. Biological Process. Description. ... and M and includes replication of the genome and the subsequent segregation of chromosomes into daughter cells. ...
studied the Start checkpoint in the G1 cell cycle phase, where cells irreversibly commit to cell division. Single-cell analysis ... The cell cycle couples growth and cell division to ensure the consistent size and shape of individual cells. This involves a ... Two reports in this issue focus on different points in the cell cycle of the budding yeast Saccharomyces cerevisiae, and find ... switch that coordinates the simultaneous transcription of a large group of cell cycle genes and the budding of a daughter cell ...
Antibodies for proteins involved in cell cycle pathways, according to their Panther/Gene Ontology Classification ...
... including cell proliferation. Herein, we demonstrate that fat mass and obesity-associated (FTO) demethylates m,sup,6,/sup,A ... FTO Demethylates Cyclin D1 mRNA and Controls Cell-Cycle Progression Cell Rep. 2020 Apr 7;31(1):107464. doi: 10.1016/j.celrep. ... m6A modification of cyclin D1 oscillates in a cell-cycle-dependent manner; m6A levels are suppressed during the G1 phase and ... Our results highlight the role of m6A in regulating cyclin D1 mRNA stability and add another layer of complexity to cell-cycle ...
failure to progress or abnormal progression through the stages of the cell cycle. ... Genes QTLs Strains Markers Genome Information Ontologies Cell Lines References Download Submit Data ...
Cell cycle machinery involves many critical factors and enzymes that need to be precisely regulated in time and space. How is ... Cell cycle is a fundamental biological process that ensures organism development and its dysregulation is linked to many human ... Cell cycle and ubiquitin signaling. Other teams from this department. * Brain development and physiology ... Fragile X-Related Protein 1 Regulates Nucleoporin Localization in a Cell Cycle-Dependent Manner. * Arantxa Agote-Arán ...
... and cell-cycle arrest. Whereas cell-cycle arrest protected HL60 cells from paclitaxel (PTX) but not from FL and DOX, Z-VAD-fmk ... Here we investigated effects of GA and 17-AAG in apoptosis-prone cells such as HL60 and U937. In these cells, doxorubicin (DOX ... Thus, by inducing Hsp70, GA protected apoptosis-prone cells in unique and cell-type selective manner. Since GA does not protect ... Also GA failed to protect HL60 cells from cytotoxicity of actinomycin D and flavopiridol (FL), inhibitors of transcription. We ...
A cell divides into two daughter cells tht are genetically identical to the original cell and to each other. Cells multiply to ... The cell divides into two daughter cells (cytokinesis). In plant cells vesicles deposit new cell wall material along the ... CELL CYCLE AND MITOSIS. Nuclear and Cytoplasmic Division in the Eukarya. Mitosis is the name for the kind of cell division that ... An acronym for the cell cycle is ...IPMATIPMATIPMATI... Most of the time a cell is in interphase, the growth and preparation ...
Click on grid cells to view annotations.. *Blue cells = expressed in wild-type.. Gray triangles = other expression annotations ...
As cells exit mitosis, the cell cycle is reset, allowing the establishment of a new, competent replication state. ... In addition to this competent complex, at least two cell cycle regulated protein kinase pathways are required to affect a ... in eukaryotic cells is a highly regulated process that leads to the duplication of the genetic information for the next cell ... As cells exit mitosis, the cell cycle is reset, allowing the establishment of a new, competent replication state. ...
Two distinct waves of cell cycle regulated genes control progression through the cell cycle: an early wave occurring during G1/ ... inhibit the expression of both the early G1/S and late G2/M cell cycle genes during G0 or the quiescent phase of the cell cycle ... p107 protein contributed to repression of the late G2/M cell cycle genes after p53 activation and during a normal cell cycle. ... We observed that DREAM and RB cooperate to repress cell cycle genes during G0 and early G1. We determined that Cyclin D-CDK4 ...
Cell cycle arrest protein BUB3. Timeline for Family b.69.4.2: Cell cycle arrest protein BUB3: *Family b.69.4.2: Cell cycle ... Family b.69.4.2: Cell cycle arrest protein BUB3 appears in SCOPe 2.01. *Family b.69.4.2: Cell cycle arrest protein BUB3 appears ... Family b.69.4.2: Cell cycle arrest protein BUB3 [110289] (2 proteins). possibly related to the WD-repeat family; both sequence ... Cell cycle arrest protein BUB3 [110290] (1 species). *. Species Bakers yeast (Saccharomyces cerevisiae) [TaxId:4932] [110291 ...
These findings show that ALS induces cell cycle arrest and promotes autophagic cell death but inhibits EMT in pancreatic cancer ... In addition, ALS suppressed the expression of sirtuin 1 (Sirt1) and pre-B cell colony-enhancing factor/visfatin in both cell ... and EMT-suppressing effects in PANC-1 and BxPC-3 cells. ALS remarkably arrested PANC-1 and BxPC-3 cells in G2/M phase via ... ALS significantly inhibited EMT in PANC-1 and BxPC-3 cells with an increase in the expression of E-cadherin and a decrease in N ...
histone cell cycle regulator (hira) gene expression in Xenopus laevis embryo. , assayed via in situ hybridization, NF stage 2, ... Throughout NF stage 2 (2-cell). animal cap. animal hemisphere. Image source: Published. Larger Image. Printer Friendly View. ...
The resumption of the mitotic cell division cycle by pheromone-arrested cells that have not mated. An example of this process ... Gene Ontology Term: re-entry into mitotic cell cycle after pheromone arrest. GO ID. GO:0000321 Aspect. Biological Process. ...
Seven days after M01ZH09 vaccination, marked cell cycle activation was identified and associated with humoral immunogenicity. ... By contrast, vaccination with Ty21a was associated with NK cell activity and validated in peripheral blood mononuclear cell ... In contrast, vaccination with Ty21a was associated with T and NK cell activity, and validated in PBMC stimulation assays ... confirming superior induction of an NK cell response. Moreover, transcriptional signatures of amino acid metabolism in Ty21a ...
... immunofluorescence or immunohistochemistry can be used to easily determine the cell cycle status. ... The cell cycle. The cell cycle has two major phases: interphase, the phase between mitotic events, and the mitotic phase, where ... Cell impermeable dyes: Fixed, permeabilized and for live/dead discrimination in intact cells. Cell permeable dyes: Intact cells ... the cells synthesize RNA and proteins to induce growth. When conditions are right, cells enter the S stage of the cell cycle ...
These videos and activities will walk them through each stage, describing what is happening to the cell and the nucleus. ... This collection will help students understand the intricacies of the cell cycle. ... cells, the cell cycle, mitosis, cell biology, cell division, cell reproduction, meiosis, dna replication, genes, dna ... This collection will help students understand the intricacies of the cell cycle. These videos and activities will walk them ...
... fungus Aspergillus nidulans we have shown that CaM is required for cell cycle progression at multiple points in the cell cycle ... Calmodulin and cell cycle control. Journal Article (Journal Article) Previous studies have indicated a role for the calcium ... A lack of calmodulin results in cell cycle arrest, and a failure in polar growth that accompanies germination of A nidulans ... Together these results indicate that calmodulin-dependent processes may be conserved between A nidulans and vertebrate cells, ...
DHM regulates cell cycle progression in SK-MEL-28 cells. To determine the effects of DHM treatment on cell cycle distribution ... Cell cycle checkpoint is an important intersection for cell survival or cell death. If conditions where cells live are ... In order to determine whether DHM has any effects on cell cycle distribution of SK-MEL-28 cells, we tested the cell cycle ... cell division cycle 25A (Cdc25A), cell division cycle 2 (Cdc2) and P-Cdc2. We found that immunoblotting of SK-MEL-28 cell ...
Unfortunately Tocriscreen Cell cycle/apoptosis (Cat. No. 1738) has been withdrawn from sale for commercial reasons. ... Keywords: Tocriscreen Cell cycle/apoptosis, Tocriscreen Cell cycle/apoptosis supplier, , Tocris Bioscience ... TocriscreenTM Cell Cycle and Apoptosis. Cat. No. 1738 Submit a Review Datasheet / COA / SDS ... Have you used TocriscreenTM Cell Cycle and Apoptosis?. Submit a review and receive an Amazon gift card.. $50/€35/£30/$50CAN/¥ ...
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We hypothesize that changes in pre-mRNA processing occurring as fibroblasts enter the proliferative cell cycle are also ... Analysis of dermal excisional wounds in mice reveals that proliferating cells adjacent to wounds express higher levels of ... e Knockdown of CstF-64 or CPSF73 reduced migration of triple negative breast cancer cells. Triple negative breast cancer cell ... The ratio of cell density in the denunded area to the non-denuded area (relative wound density) over a time-course is plotted. ...
... ... The aim of this study is to evaluate the prognostic value in GIST of some oncoproteins involved in regulation of cell ...
Two recently discovered transcription factors stop cells from dividing when plants face extreme heat and DNA damage. ... Plant Stress: Hitting pause on the cell cycle. Two recently discovered transcription factors stop cells from dividing when ... While signalling pathways that inhibit cell cycle progression have been elucidated, the putative core module orchestrating cell ... and even trigger cell death in response to DNA damage (Kastenhuber and Lowe, 2017). Many cell cycle and DNA repair genes are ...
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  • Our results show that cell cycle progression explains less than half of all cell-to-cell variability, and that most cycling proteins are regulated post-translationally, rather than by transcriptomic cycling. (
  • Progression through the phases of the mitotic cell cycle, the most common eukaryotic cell cycle, which canonically comprises four successive phases called G1, S, G2, and M and includes replication of the genome and the subsequent segregation of chromosomes into daughter cells. (
  • To cope with these stress conditions, cells have developed a set of surveillance mechanisms that monitor the status and structure of DNA during cell cycle progression. (
  • Herein, we demonstrate that fat mass and obesity-associated (FTO) demethylates m 6 A modification of cyclin D1, the key regulator for G1 phase progression and controls cell proliferation in vitro and in vivo. (
  • Using a molecular genetic approach in the filamentous fungus Aspergillus nidulans we have shown that CaM is required for cell cycle progression at multiple points in the cell cycle. (
  • Transduced p16INK4a peptides inhibit hypophosphorylation of the retinoblastoma protein and cell cycle progression prior to activation of Cdk2 complexes in late G1. (
  • It is concluded that cyclin D:Cdk4/6 activity is required for early G1 phase cell cycle progression up to, but not beyond, activation of cyclin E:C DK2 complexes at the restriction point and is thus nonredundant with cyclin Cdk2 in late G1. (
  • Inhibition of pRb phosphorylation and cell cycle progression by an antennapedia-p16(INK4A) fusion peptide in pancreatic cancer cells. (
  • This roller coaster ride, or oscillation, of gene expression is essential for the proper progression through the cell cycle to allow accurate DNA replication and cell division. (
  • Furthermore, we will discuss the functional impact of E2Fs on the cell cycle progression and outline the consequences when E2F expression is disturbed. (
  • Here, we set out to investigate the effect of VACV infection on cell proliferation and host cell cycle progression. (
  • We conclude that VACV modulates host cell proliferation and host cell cycle progression through temporal expression of multiple VACV effector proteins. (
  • We recently recognized a previously uncharacterized linkage between the replication stress response and the SCF ubiquitin-proteasome pathway (Kile and Koepp 2010) a system that is better known for its part in protein turnover during cell-cycle progression (Ang and Harper 2005). (
  • What is known is that shifts in the cell membrane potential are essential for cell cycle progression and that VGSCs and Na + ,K + -ATPase play an important role in this process [15]. (
  • These findings indicate that Shh and PI3K signaling pathways converge on N-Myc to regulate neuronal precursor cell cycle progression. (
  • Natural substances exert their anti-cancer activity by modulating cell cycle progression and inducing apoptosis-regulatory proteins ( 8 , 9 ). (
  • Expression of p27 by transfection substantially reduced cell cycle progression, and its activity was enhanced by mutations designed to stabilize the protein. (
  • A checkpoint is one of several points in the eukaryotic cell cycle at which the progression of a cell to the next stage in the cycle can be halted until conditions are favorable. (
  • Here we have identified the Fkh2 transcription factor as a regulatory target of both Cdc28 and the cell wall biosynthesis kinase Cbk1, in a role distinct from its conserved function in cell cycle progression. (
  • We also show that Smo ablation disrupts cell cycle regulator CyclinD1 and leads to abnormal cell cycle progression through G1 to S transition. (
  • NDRG4 is required for cell cycle progression and survival in glioblastoma cells. (
  • As a result of these effects on cell cycle progression and survival, NDRG4 knockdown decreases the tumorigenic capacity of established GBM cell lines and GBM CSC-enriched cells that have been implanted intracranially into immunocompromised mice. (
  • Collectively, these data indicate that NDRG4 is required for cell cycle progression and survival, thereby diverging in function from its tumor suppressive family member NDRG2 in astrocytes and GBM cells. (
  • We also found that THU regulates cell cycle progression at the G1/S checkpoint by suppressing E2F1. (
  • Introduction The ability to rapidly delay cell cycle progression in response to environmental and genotoxic insults, is essential for the maintenance of genomic integrity and/or cell viability. (
  • In this study, we have investigated the effect of caffeine on Cdc25 stability, cell cycle progression and DNA damage/replication DMA checkpoint activation in cells (Fig. (
  • Dysregulation of the cell-cycle machinery and activation of cyclin-dependent kinases (CDKs) to promote cell-cycle progression is a key mechanism in many cancer pathologies. (
  • First, we combine single cell data and stochastic modeling and, secondly, we use a transcriptome-wide approach for deletion mutants of the main G1/S transition regulators to understand the importance of these regulators for cell cycle progression and periodic genes expression. (
  • Next they tested the requirement of ERK activity on cell cycle progression in vivo . (
  • PD0325901 administration reduced the number of mVenus+ cells in S/G2/M, indicating that ERK activity is required for G1/S progression in vivo . (
  • In this chapter, we introduce robust and straightforward methods to analyze cell cycle progression in S. cerevisiae. (
  • These techniques can be utilized to describe cell cycle events and to address the effects of perturbations on accurate and timely cell cycle progression. (
  • Identification of a novel centrosome/microtubule-associated coiled-coil protein involved in cell-cycle progression and spindle organization. (
  • The progression of the cell cycle is controlled by a complex interplay among various cell cycle regulators. (
  • Our Cell Meter™ Fluorimetric Cell Cycle Assay Kits are designed to monitor cell cycle progression and proliferation by using our proprietary cell cycle dye in permeabilized and fixed cells. (
  • As such, mechanism(s) that regulate cardiomyocyte cell cycle progression have been the focus of intense research over the past two decades. (
  • Regulation of DNA-replication origins during cell-cycle progression. (
  • We study the effects of a DNA-damaging agent, methyl methane sulphonate (MMS), and of mutations in checkpoint genes such as rad53 on the activity of origins, measured by two-dimensional gel analysis, and on cell-cycle progression, measured by fluorescence-activated cell sorting. (
  • However, the specific, targeted mechanism of Aurora A kinase inhibitors makes their use in combination with an agent that may enhance apoptotic activity in cancer cells that have undergone abnormal mitotic progression one of great interest. (
  • CST has a diverse catalog of antibodies and assays to study cell cycle progression and checkpoint control. (
  • it is shown here that caffeine does not override the radiomimetic delay imposed by TPA in HeLa, but instead enhances it, without affecting G2 progression in control cells. (
  • Most of the other agents which more specifically affect some of the diverse range of caffeine targets either do not affect G2 progression after TPA, or delay G2 progression in control cells and exert a further delay in the presence of TPA. (
  • The exception is 2-aminopurine, a protein kinase inhibitor which has been shown to have an action similar to that of caffeine is allowing progression of the cell cycle to mitosis after the inhibition of DNA synthesis, without affecting normal cycle progression through G2. (
  • This agent, like caffeine, also has the contrary action of retarding cycle progression after TPA. (
  • These delayed initiations and interruption of treatment cycles resulted in increased stress, anxiety, disease progression, recurrence and premature death. (
  • This spatially resolved proteomic map of the cell cycle is integrated into the Human Protein Atlas and will serve as a resource for accelerating molecular studies of the human cell cycle and cell proliferation. (
  • The group aims to understand how cell-cycle control genes drive plant cell proliferation, and to elucidate how cell division control interacts with different aspects of plant development, such as morphogenesis, architecture and growth, both under control and stress conditions. (
  • In most regenerative systems, regeneration is controlled through activated cell proliferation in response to an injury-induced release of a mitogenic signal. (
  • N 6 -Methyladenosine (m 6 A) modification is the major chemical modification in mRNA that controls fundamental biological processes, including cell proliferation. (
  • Flavonoids potently inhibited of A549 cells in a dose-dependent manner, whereas flavonoids had a weak inhibitory effect on proliferation of WI-38 cells. (
  • Deubiquitinating enzymes (DUBs) are important regulators of cell proliferation. (
  • Enforced expression of OTUD-6B in Ba/F3 cells could block cell proliferation by arresting cells in G1 phase. (
  • Therefore, down-regulation of Otud-6b expression after prolonged cytokine stimulation may be required for cell proliferation in B lymphocytes. (
  • However, ubiquitylation of substrate proteins can also result in non-proteolytic events and plays important functions in many biological processes including cell proliferation. (
  • Embryogenesis requires an exquisite regulation of cell proliferation, cell cycle withdrawal and differentiation into a massively diverse range of cells at the correct time and place. (
  • Therefore, regulated proliferation and subsequent differentiation of stem and progenitor cells remains pivotal throughout life. (
  • Recent advances have characterised the cell cycle dynamics, epigenetics, transcriptome and proteome accompanying the transition from proliferation to differentiation, revealing multiple bidirectional interactions between the cell cycle machinery and factors driving differentiation. (
  • We discuss examples from the three embryonic germ layers to illustrate this regulatory mechanism that co-ordinates the balance between cell proliferation and differentiation. (
  • Previous studies have indicated a role for the calcium receptor calmodulin in the control of eukaryotic cell proliferation. (
  • Together these results indicate that calmodulin-dependent processes may be conserved between A nidulans and vertebrate cells, and suggest that this approach may allow us to elucidate the molecular mechanism underlying calmodulin-regulated control of cell proliferation. (
  • The aim of the present study was to evaluate the effects of DHM on cell proliferation, cell cycle distribution and apoptosis in the human melanoma SK-MEL-28 cell line, and to explore the related mechanisms. (
  • The effect of DHM on cell proliferation was investigated by MTT assay, and cell cycle distribution was determined by flow cytometry. (
  • The results revealed that DHM suppressed cell proliferation of SK-MEL-28 cells in a concentration- and time-dependent manner, and caused cell cycle arrest at the G1/S phase. (
  • B) Cell proliferation of SK-MEL-28 cells was apparently suppressed in a concentration- and time-dependent manner after 48 or 72 h of incubation with DHM. (
  • A previous study confirmed that DHM inhibits the cell proliferation and metastasis of prostate cancer in vitro and in vivo ( 14 ). (
  • DHM sodium was shown to inhibit the proliferation of bladder carcinoma, and its molecular mechanism was partially attributed to cell cycle arrest ( 15 ). (
  • In addition, DHM suppressed the proliferation of hepatoma cells by inhibiting angiogenesis via downregulation of vascular endothelial growth factor and basic fibroblast growth factor expression ( 17 , 18 ). (
  • The regulation of cell cycle and proliferation has been extensively studied in the last few years and a consensus paradigm of cell cycle regulation has been developed [1,2]. (
  • The aim of this study is to evaluate the prognostic value in GIST of some oncoproteins involved in regulation of cell proliferation. (
  • Using a subset of VACV mutants, we characterise the stage of infection required for inhibition of cell proliferation and define the viral effectors required to dysregulate the host cell cycle. (
  • The aim of this study was to determine the global transcriptome profile of three passages of dermal autologous fibroblasts from a male volunteer, focusing on the processes of the cell cycle and cell proliferation status to estimate the optimal passage of the tested cells with respect to their reimplantation. (
  • Detailed microarray analysis of the fibroblast genes indicated that the cell population of the third passage exhibited the highest number of upregulated genes involved in the cell cycle and cell proliferation. (
  • Developmental programs that coordinate neuronal precursor proliferation and cell cycle exit are poorly understood. (
  • FCP displayed concentration-dependent inhibition on A549 cells proliferation. (
  • Cell proliferation regulation is a central part of the tissue morphogenesis process during the development of multicellular organisms. (
  • As the patient base of a number of cancers continue to expand at an enormous pace across the globe, a great need is being felt for the investigation of cell proliferation and measure the proportion of sells in every phase of the cell cycle of the cell under observation. (
  • As a cell's decision regarding proliferation is made in the G1 phase of development, immediately before the initiation of the process of DNA synthesis and before the rest of the cell cycle progresses, researchers state that the detection of DNA synthesis of a cell at this stage helps in the unambiguous determination of the status of growth regulation in experiments related to cell culture. (
  • ERRβ is a regulator of cell cycle and inhibition of ERRβ leads to cell proliferation. (
  • Accumulating evidence indicates that proliferation and cell fate specification of neural progenitor cells are regulated by both cell-intrinsic factors and cell-extrinsic cues. (
  • Among the known growth factors, the Hedgehog family of molecules has been shown to regulate neural tissue patterning, cell proliferation, laminar organization, and neuronal differentiation in the vertebrate retina. (
  • These molecular genetic analyses thus reveal specific functions and the critical timing of Hedgehog signaling for neuronal differentiation and cell proliferation in the mammalian retina. (
  • Given this tissue-specific expression pattern and the established tumor suppressive roles of the NDRG family in regulating cellular proliferation, we investigated the cellular and biochemical functions of NDRG4 in the context of astrocytes and glioblastoma multiforme (GBM) cells. (
  • Three different carcinoma cell lines (MIAPaCa-2, H441, and H1299) exhibited decreased cell proliferation after sole administration of THU, while being unaffected by knocking down CDA. (
  • Similarly, Ki-67 staining further supported that THU reduces cell proliferation. (
  • HepG2.2.15 cells showed decreased proliferation ability compared to HepG2 cells. (
  • Our results suggested that HBV inhibited the capability of proliferation of HepG2.2.15 cells by regulating cell cycle genes expression and inducing G1 arrest. (
  • This study focused on the cell cycle control and further investigated how HBV influenced the ability of proliferation in HepG2.2.15 cells. (
  • Cell Proliferation , 30 (10-12), 457. (
  • In this preprint, the authors used transgenic mice containing satellite cell-specific Förster/fluorescence resonance energy transfer (FRET) biosensors and cell-cycle reporters to explore how extracellular signal-regulated kinase (ERK) signaling contributes to satellite cell proliferation and migration during endogenous repair. (
  • There are a variety of parameters that can be used for monitoring cell viability and proliferation. (
  • Any misstep in this regulatory cascade causes abnormal cell proliferation which underlies many pathological conditions, such as tumor formation. (
  • WNT/β-Catenin pathway is an evolutionarily conserved signaling pathway with essential roles in cell proliferation and differentiation. (
  • Moreover, GOF animals did not show an increase in mitotic cardiomyocytes by means of pH3 immunostaining (although there was a trend towards increase, with considerable variability), a mitosis marker considered a gold standard for assessment of cardiomyocyte cell cycle entry, indicating that increased canonical WNT signaling may not be sufficient to induce cardiomyocyte proliferation under basal conditions. (
  • In contrast to the deregulated hepatocellular division that is a feature of many hepatic diseases and malignancies, physiologic liver growth during embryonic development and after partial hepatectomy (PH) in adults is characterized by tightly controlled cell proliferation. (
  • Disruptions to the cell cycle that governs proliferation are a root cause of many diseases, most notably cancer. (
  • Inappropriate CDC25C regulation could mechanistically underlie TRIB2 mediated regulation of cellular proliferation in neoplastic cells. (
  • or physiological or as a description of key events and processes starting toxic effects that affect cell proliferation. (
  • In vitro studies based on MCF-7 cell proliferation and induction of vitellogenin in primary culture of rainbow trout hepatocytes. (
  • it is often a biochemical alternative to the self-destruction of such a damaged cell by apoptosis. (
  • Induction of the cell cycle arrest and apoptosis by flavonoids isolated from Korean Citrus aurantium L. in non-small-cell lung cancer. (
  • These results clearly indicated that the anti-cancer effect of flavonoids on A549 cells follows multiple cellular pathways through G2/M arrest and the induction of apoptosis. (
  • Here we investigated effects of GA and 17-AAG in apoptosis-prone cells such as HL60 and U937. (
  • In these cells, doxorubicin (DOX) caused rapid apoptsis, whereas GA-induced heat-shock protein-70 (Hsp70) (a potent inhibitor of apoptosis) and G1 arrest without significant apoptosis. (
  • GA blocked caspase activation and apoptosis and delayed cell death caused by DOX. (
  • Whereas cell-cycle arrest protected HL60 cells from paclitaxel (PTX) but not from FL and DOX, Z-VAD-fmk prevented FL-induced apoptosis but was less effective against DOX and PTX. (
  • Thus, by inducing Hsp70, GA protected apoptosis-prone cells in unique and cell-type selective manner. (
  • Since GA does not protect apoptosis-reluctant cancer cells, we envision a therapeutic strategy to decrease side effects of chemotherapy without affecting its therapeutic efficacy. (
  • Chemotherapy causes apoptosis in certain cancer and normal cells, leading to both therapeutic and side effects. (
  • Broadly, all cells could be subdivided into apoptosis-prone and reluctant. (
  • As a canonical example, HL60 cells are apoptosis prone. (
  • 7 For example, K562 leukemia cells are apoptosis reluctant, because they express the Bcr-Abl antiapoptotic kinase, which in turn induces heat-shock protein-70 (Hsp70). (
  • Tocriscreen TM Cell Cycle and Apoptosis (Cat. (
  • A collection of 52 high purity compounds with defined biological actions in the field of cell cycle and apoptosis research. (
  • Currently there are no citations for Tocriscreen TM Cell Cycle and Apoptosis. (
  • Be the first to review Tocriscreen TM Cell Cycle and Apoptosis and earn rewards! (
  • Have you used Tocriscreen TM Cell Cycle and Apoptosis? (
  • Additionally, DHM significantly induced the apoptosis of SK-MEL-28 cells, and enhanced the expression levels of Bax proteins and decreased the protein levels of IKK-α, NF-κB (p65) and P-p38. (
  • Regardless of mitogens used, proliferating mammary epithelial cells show comparable p53 responses to gamma-irradiation, including expression of nuclear p53 and p21/WAF1 and increased levels of apoptosis, compared to non-proliferating irradiated control cultures. (
  • Cell Cycle Multiple Choice Questions and Answers (MCQs) PDF download, a book to practice quiz questions and answers on 9th grade biology topics: Introduction to cell cycle, chromosomes, meiosis, phases of meiosis, mitosis, significance of mitosis, apoptosis, and necrosis tests for high school students and beginners. (
  • We found that LCs do not undergo apoptosis following IR as do other dendritic cell (DC) subsets but instead persist and migrate to skin-draining lymph nodes. (
  • Additionally, we found that the cell cycle regulator p21 is overexpressed in LCs at rest and that in contrast to WT LCs, p21−/− LCs undergo apoptosis, accumulate significant DNA damage, and fail to experience cell cycle arrest following IR. (
  • The genes contributing to the significantly different gene sets in the subjects given fish oil compared with the control group are involved in cell cycle, endoplasmic reticulum (ER) stress and apoptosis. (
  • The increased expression of genes related to cell cycle, ER stress and apoptosis suggests that intake of fish oil may modulate basic cellular processes involved in normal cellular function. (
  • These findings suggest that FCP induced G2/M arrest and apoptosis of A549 cells. (
  • Apoptosis is a type I programmed cell death that is characterized by distinct phenotypes from necrosis, including membrane blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation and apoptotic body formation ( 10 , 11 ). (
  • In addition, B-cell lymphoma (Bcl)-2 family proteins are important for apoptosis regulation, which could be either proapoptotic, such as Bcl-2-associated X protein (Bax) or Bcl-2 homologous antagonist/killer, or antiapoptotic, such as Bcl-2 and Bcl-extra large (Bcl-xL) ( 13 ). (
  • Neurons initiate but do not complete cell division, eventually entering apoptosis. (
  • The first hit is abnormal cell cycle reentry, which typically results in neuronal apoptosis and prevention of AD. (
  • However, with the second hit of chronic oxidative damage preventing apoptosis, neurons gain "immortality" analogous to tumor cells. (
  • Background: Recent experimental evidence suggests that DNA damage and cell cycle regulatory proteins are involved in kidney injury and apoptosis. (
  • While NDRG4 overexpression has no effect on cell viability, NDRG4 knockdown causes G(1) cell cycle arrest followed by apoptosis. (
  • Damage is lethal only if it exceeds a cell's tolerance threshold at one or more checkpoints in the cell cycle (for apoptosis) or at any time point (for necrosis). (
  • In order to explore the potential mechanism, cell cycle and apoptosis were analysed. (
  • Although, if unrepairable, the cell will program its own death (apoptosis). (
  • Potential applications for live-cell studies are in the determination of cellular DNA content and cell cycle distribution for detecting variations in growth patterns, for monitoring apoptosis, and for evaluating tumor cell behavior and suppressor gene mechanisms. (
  • The percentage of cells in a given sample that are in G0/G1, S and G2/M phases, as well as the cells in the sub-G1 phase prior to apoptosis can be monitored with a flow cytometer. (
  • After a certain number of cell divisions, the telomeres become so short that they trigger the cell to stop dividing or to self-destruct (undergo apoptosis). (
  • Telomerase allows these cells to divide many times without becoming damaged or undergoing apoptosis. (
  • For the cell-division cycle to progress, hundreds of genes and proteins must be coordinately regulated. (
  • The CDK network directly or indirectly orchestrates coordinated regulation of proteins and genes involved in essentially every aspect of cell function. (
  • The cell cycle is driven by precise regulation of proteins in time and space, which creates variability between individual proliferating cells. (
  • We show that around one-fifth of the human proteome displays cell-to-cell variability, identify hundreds of proteins with previously unknown associations with mitosis and the cell cycle, and provide evidence that several of these proteins have oncogenic functions. (
  • These proteins are disproportionately phosphorylated by kinases that regulate cell fate, whereas non-cycling proteins that vary between cells are more likely to be modified by kinases that regulate metabolism. (
  • Flow cytometry and Western blot analysis showed that flavonoids induced cell cycle arrest at the G2/M checkpoint by controlling the proteins expression level of cyclin B1, cdc2, cdc25c and p21(WAF1/CIP1). (
  • Chromosomes (now single molecules of DNA with associated proteins) have reached opposite poles of the cell. (
  • During the first stage called G1, cells monitor their environment and, when the requisite signals are received, the cells synthesize RNA and proteins to induce growth. (
  • As cells go through the phases of the cell cycle, proteins such as histone H3 Ser28 become modified or change in expression. (
  • To further support the study of cell cycle, BD Biosciences carries antibodies to these proteins to use for imaging or flow cytometry applications. (
  • DHM increased the production of p53 and p21 proteins and downregulated the production of Cdc25A, Cdc2 and P-Cdc2 proteins, which induced cell cycle arrest. (
  • If stabilized, these proteins maintain the cells in the phase just before division (G2/M arrest) by binding to and repressing the genes essential for cell division to proceed. (
  • These alterations in cell cycle were associated with changes in cell cycle regulatory proteins and other cell cycle associated proteins. (
  • Migration through constrictions can clearly rupture nuclei and mis-localize nuclear proteins but damage to DNA remains uncertain as does any effect on cell cycle. (
  • Growth factor proteins arriving at the dividing cell's plasma membrane can trigger the cell to begin dividing. (
  • negative regulator molecules, such as tumor suppressor proteins, monitor cellular conditions and can halt the cycle until specific requirements are met. (
  • The cell cycle of eukaryotes is regulated by expression and activation of molecules known as cell division cycle (cdc) proteins. (
  • In addition, rat lung proteins prepared from uninfected rats using identical methods and immunoprecipited with anti-PSTAIR failed to show any significant kinase activity, verifying that the protein kinase activity was derived from the PC cdcZ homologue and was not a host cell contaminant. (
  • Additionally, we are improving methods for the visualization of single mRNAs and proteins inside living cells. (
  • Intravital two-photon microscopy (IVM) enables the real-time visualisation of cells within living tissues, by tracking fluorescently labelled cells and/or proteins within an 'imaging window' of anaesthetised animals. (
  • The study was conducted to assess the p53-dependent and -independent effects of the proto-oncogene MDMX in regulating major proteins of cell cycle and angiogenesis in prostate cancer (PCa). (
  • Proteins called cyclins and CDKs coordinate with each other and control when cells divide. (
  • We are particularly interested in disease associated proteins involved in cilia formation and cell division, and in the mechanism(s) that regulate centrosome composition in response to radiation. (
  • By studying disease-associated centrosomal/ciliary proteins in cell line models and patient biopsies, we aim at a mechanistic understanding of their function at a molecular level, and at the identification of candidate biomarkers or targets for mono- and radiation-combination therapy. (
  • The two gap phases provide time for the cell to grow and double the mass of their proteins and organelles. (
  • The cell's passage through cell cycle is controlled by a host of different regulatory proteins. (
  • These regulators activate transcription factors, which bind to DNA and turn on or off the production of proteins that result in cell division. (
  • During interphase, a cell increases in size, synthesis new proteins and organelles, replicates its chromosomes , and prepares for cell division by producing spindle proteins. (
  • This revealed an unexpectedly broad response, with proteins related to distinct cell cycle events undergoing simultaneous phosphoregulation. (
  • G1 is now termed as the first growth phase as it involves the synthesis of other components of the cell such as RNA (Ribose Nucleic Acid), membranes, and proteins which lead to the growth of cytoplasm and nucleus of the daughter cells to get their mature size. (
  • Proteins like kinases and cyclins are critical for the cell cycle. (
  • Studying the dynamic nature and contribution of cytoskeletal and ECM proteins to cell structure and motility can provide insight into cell migration in the tumor microenvironment, metastasis, and neurodegeneration. (
  • Maintaining homeostasis requires cells to regulate the translation, stability and degradation of thousands of proteins simultaneously. (
  • In this part of interphase, the cell synthesizes mRNA and proteins in preparation for subsequent steps leading to mitosis. (
  • F/G group (single-cycle infectious virions with NiV B F and G proteins on the cell surface). (
  • These events include the duplication of its DNA (DNA replication) and some of its organelles, and subsequently the partitioning of its cytoplasm, chromosomes and other components into two daughter cells in a process called cell division. (
  • To ensure the proper replication of cellular components and division, there are control mechanisms known as cell cycle checkpoints after each of the key steps of the cycle that determine if the cell can progress to the next phase. (
  • The B period extends from the end of cell division to the beginning of DNA replication. (
  • The D period refers to the stage between the end of DNA replication and the splitting of the bacterial cell into two daughter cells. (
  • In eukaryotes, the cycle is divided into four phases: cell growth in G1 phase, DNA replication in S phase, more growth in G2 phase, and cell division in mitosis or M phase. (
  • In some variant cell cycles nuclear replication or nuclear division may not be followed by cell division, or G1 and G2 phases may be absent. (
  • The initiation of DNA replication in eukaryotic cells is a highly regulated process that leads to the duplication of the genetic information for the next cell generation. (
  • As cells exit mitosis, the cell cycle is reset, allowing the establishment of a new, competent replication state. (
  • Cell growth, replication and division in eukaryotic cells occur according to a highly controlled series of events called the cell cycle. (
  • When something goes awry during the cell cycle - for example, if DNA gets broken during replication - checkpoint mechanisms put the cycle on pause so that the cell can repair the damage before dividing. (
  • To facilitate viral genome replication, vaccinia virus (VACV) has been reported to alter cell cycle regulation and trigger the host cell DNA damage response. (
  • Consistent with the data showing hyperactivation of Rad53 in cells DNA replication is definitely sluggish in cells in the presence of MMS (Blake 2006). (
  • A large proportion of epithelial cells of the terminal duct lobular unit reside in a primed 'replication licensed' but not proliferating state. (
  • We have known for decades that ion channels and shifts in membrane potential play important roles in the cell cycle that are responsible for preparing the cell for the sequence of events that must take place to ensure maintenance, replication and survival, through control of constantly changing intra- and extracellular ion concentrations [15]. (
  • This process includes mechanisms to ensure errors are corrected while cell replication occurs, and if the correction cannot be performed, cells enter into the apoptotic process ( 15 ). (
  • Both the initiation and inhibition of cell division are triggered by events external to the cell when it is about to begin the replication process. (
  • However, little is known about the impacts of the complete HBV genome or HBV replication on host cells. (
  • 2. Design of a self oscillating model of the complete cell cycle with predefined points for external interaction (like different stresses) and interaction points for other cellular processes or components like metabolism or the DNA replication machinery. (
  • We are focusing on the G1/S transition also called START in S. cerevisiae and known as the point of no return, meaning once cells pass this checkpoint they initiate DNA replication and have to pass through the entire cell cycle. (
  • Cell division is strictly controlled by an intricate signaling system that synchronizes three different duplication events: DNA replication, nuclear division and cell division, hence ensuring ordered duplication and separation. (
  • G1 is an intermediate phase occupying the time between the end of cell division in mitosis and the beginning of DNA replication during S phase. (
  • The DNA damage checkpoint pathway enforces cell cycle arrest to allow timely repair in response to DNA damage and replication stress. (
  • Any DNA replication initiation that is involved in cell cycle DNA replication. (
  • Before a cell begins DNA replication, it has to make certain it prepared to take on such a strategy. (
  • If the checkpoint mechanisms detect problems with the DNA, the cell cycle is halted, and the cell attempts to either complete DNA replication or repair the damaged DNA. (
  • G 1 , S, G 2 , and M . The S or synthesis phase is when DNA replication occurs, and the M or mitosis phase is when the cell actually divides. (
  • During this time, the cell grows in preparation for DNA replication, and certain intracellular components, such as the centrosomes undergo replication. (
  • The protein, CDT1, helps facilitate DNA replication during the initial part of the cell cycle, called interphase, during which DNA is replicated and checked for errors, before being separated into two daughter cells in the latter part of the cell cycle, called mitosis. (
  • We have shown previously that chromosome VI of Saccharomyces cerevisiae contains nine origins of DNA replication that differ in initiation frequency and replicate sequentially during the S phase of the cell cycle. (
  • We conclude that rad53 regulates the timing of initiation of replication from late origins during normal cell growth and blocks initiation from late origins in MMS-treated cells. (
  • In response to replication stress, ATR has been shown to mediate a global cellular response that promotes cell cycle arrest, inhibition of late source firing, stabilization of replication forks, transcriptional rules and DNA restoration (11,12). (
  • In LR-90 addition, ATR-CHK1 signaling takes on a prominent part in controlling E2F-dependent transcription (16C18), which includes a large set of genes with important tasks in DNA replication, DNA repair and cell cycle control (19). (
  • Alternation of chromosome replication and segregation is essential for successful completion of the cell cycle and it requires an oscillation of Cdk1 (cyclin-dependent kinase 1)-CycB (cyclin B) activity. (
  • Which phase of the cell cycle does replication take place? (
  • The replication cycle of HIV occurs exclusively within infected cells, although HIV may also be found extracellularly when new progeny viruses are released from the cell by budding. (
  • M phase is itself composed of two tightly coupled processes: mitosis, in which the cell's nucleus divides, and cytokinesis, in which the cell's cytoplasm divides forming two daughter cells. (
  • A cell divides into two daughter cells tht are genetically identical to the original cell and to each other. (
  • at the end of mitosis, the cell plate divides the two daughter cells. (
  • The cell divides into two daughter cells (cytokinesis). (
  • The cell cycle has two major phases: interphase, the phase between mitotic events, and the mitotic phase, where the mother cell divides into two genetically identical daughter cells. (
  • The cell cycle is controlled by a complex series of signaling pathways by which a cell grows, replicates its DNA and divides ( 14 ). (
  • The Chs2p chitin synthase lays down the primary septum, which divides mother and daughter yeast cells. (
  • For varying-schedule exposures, cell heterogeneity and cycle asynchrony necessitate a cell-cycle-phase-structured model that divides the population into cohorts with different responses, still determined for each cohort by the peak additive damage model, that are then averaged. (
  • Cell cycle or the cell division is the biological process during which a cell divides for the formation of daughter cells. (
  • In a growing cell each unravelled chromosome is producing a copy of itself so that there will be a chromosome for each of the two new daughter cells when the cell divides, or reproduces itself. (
  • So when the cell divides in two to make two new cells, each chromatid becomes a chromosome in one of the new cells. (
  • The cell cycle is the life cycle of a cell, as it grows, replicates its chromosomes, separates its chromosomes and divides. (
  • Organelles such as the mitochondria and chloroplasts are replicated during this time so that when the cell divides into two new cells, each new cell will have enough organelles. (
  • Binary Fission -Asexual reproduction in single-celled organisms that happens when a single cell divides in half resulting in two new cells that are genetically identical to the original parent cell. (
  • The stage of the cell cycle where the rest of the cell divides after mitosis is complete. (
  • A cell divides and produces new cells in a series of stages. (
  • Four haploid daughter cells are formed when a single cell divides twice. (
  • The cell then divides in two and each new cell enlarges to the original size. (
  • The cell cycle in prokaryotes is quite simple: the cell grows, its DNA replicates, and the cell divides. (
  • In most cells, telomeres become progressively shorter as the cell divides. (
  • Telomerase counteracts the shortening of telomeres by adding small repeated segments of DNA to the ends of chromosomes each time the cell divides. (
  • The second phase is the mitotic phase (M-Phase) during which the cell divides and transfers one copy of its DNA to two identical daughter cells. (
  • After the division of nucleus, constriction of cytoplasm takes place which divides the cell into two daughter cells. (
  • An active eukaryotic cell will undergo these steps as it grows and divides. (
  • Before a cell divides and DNA is passed from one cell to another, a complex process occurs. (
  • In cells with nuclei (eukaryotes, i.e., animal, plant, fungal, and protist cells), the cell cycle is divided into two main stages: interphase and the mitotic (M) phase (including mitosis and cytokinesis). (
  • During interphase, the cell grows, accumulating nutrients needed for mitosis, and replicates its DNA and some of its organelles. (
  • After cell division, each of the daughter cells begin the interphase of a new cell cycle. (
  • Although the various stages of interphase are not usually morphologically distinguishable, each phase of the cell cycle has a distinct set of specialized biochemical processes that prepare the cell for initiation of the cell division. (
  • The eukaryotic cell cycle consists of four distinct phases: G1 phase, S phase (synthesis), G2 phase (collectively known as interphase) and M phase (mitosis and cytokinesis). (
  • Interphase is a series of changes that takes place in a newly formed cell and its nucleus before it becomes capable of division again. (
  • Typically interphase lasts for at least 91% of the total time required for the cell cycle. (
  • The cell cycle refers to the continuing series of divisions alternating with cell growth: interphase mitosis interphase mitosis interphase. (
  • Most of the time a cell is in interphase , the growth and preparation stage of the cycle. (
  • then the daughter cells enter interphase. (
  • This is like the reverse of prophase the cell is returning to interphase. (
  • Whatever the source of the message, the cell receives the signal, and a series of events within the cell allows it to proceed into interphase. (
  • Together with other Golgi matrix components, GRASP65 contributes to the stacking of Golgi cisternae in interphase cells. (
  • Here we show that GRASP65 is phosphorylated on serine 277 in interphase cells, and this is strongly enhanced in response to the addition of serum or epidermal growth factor. (
  • Interphase is the longest part of the cell cycle. (
  • The first part of Interphase involves cell growth and is called the Gap 1 Phase or the G 1 -Phase . (
  • During this part of Interphase, the chromosomes located in the nucleus are copied or replicated as the cell prepares to divide. (
  • The MCQs on 'Cell Cycle' will help you to understand the definition and basic stages of cell cycle and detailed description of interphase. (
  • During interphase, the cell undergoes normal growth processes while also preparing for cell division. (
  • The cell cycle is composed of 3 main stages - interphase, mitosis and cytokinesis . (
  • During the interphase stage of the cell cycle, the cell grows and organelles such as mitochondria and ribosomes double. (
  • Together, interphase and cell division make up the cell cycle. (
  • The five stages of cell cycle are - interphase , which is in turn classified into G1, S and G2 phase, Mitosis, also called as the M phase, which is further divided into 4 parts (prophase, metaphase, anaphase and telophase) and Cytokinesis. (
  • The first stage is interphase during which the cell grows and replicates its DNA. (
  • Following interphase, the cell enters mitosis or meiosis, which leads to cell division (cytokinesis) and the beginning of a new cell cycle in each of the daughter cells. (
  • G2 phase, Gap 2 phase, or Growth 2 phase, is the third subphase of interphase in the cell cycle directly preceding mitosis. (
  • Interphase lasts for 95% of the duration of the cell cycle. (
  • During the mitotic phase, the replicated chromosomes, organelles, and cytoplasm separate into two new daughter cells. (
  • Mitosis, or cell division, involves a duplication of the chromosomes of the mitotic cell, which are subsequently distributed between two daughter cells. (
  • The chromosomes assemble on the equatorial plate (an imaginary disc that crosses the center of the 3-dimensional cell). (
  • Sister chromatids have separated from each other, and they, as new chromosomes, are moving to opposite poles of the cell. (
  • Mistakes in the duplication or distribution of the chromosomes lead to mutations that may be passed forward to every new cell produced from an abnormal cell. (
  • In all eukaryotic cells, DNA is packaged into multiple chromosomes that are linked to microtubules through a large protein complex called a kinetochore. (
  • Our findings suggest that the presence of tau protein is involved in separation of sister chromatids in anaphase, and that tau protein also participates in maintaining the integrity of the DNA (pT231, prophase) and chromosomes during cell division (TG-3). (
  • This can happen if the chromosomes are incorrectly distributed to a new cell. (
  • There are 23 pairs of chromosomes in a human cell but we will follow 3 chromosomes for simplicity. (
  • The chromosomes only take on a recognisable shape when the cell is ready to divide. (
  • In a cell the chromosomes are usually not recognisable - the DNA is unravelled in the nucleus . (
  • After the chromosomes take shape they line up together (at the metaphase plate) between two ends, or poles, of the cell. (
  • Cell division complete, the chromosomes unravel and copy themselves again ready for the next cell division. (
  • By the end of mitosis, the sister chromatids have separated from each other and the original chromosomes and their copies form the nuclei of two new cells. (
  • This means that the two new cells resulting from mitotic division have the same number of chromosomes as the original cell. (
  • During the cell cycle chromosomes duplicate so that each cell has the same amount of DNA after cell division. (
  • If a cell has 24 chromosomes, how many chromosomes will each of its daughter cells have after mitosis? (
  • The reason this cycle exists is in order for the cell to accurately duplicate the large amount of DNA located in the chromosomes and to segregate two copies inside two identical daughter cells. (
  • Cancer cells have quantities of mutations or chromosomes in chromosomes. (
  • The chromosomes are pulled by the axis of the cell. (
  • Prometaphase: chromosomes attach to microtubules and chromosomes move to the equator of the cell. (
  • Metaphase: chromosomes are aligned along the center of the cell in a straight line. (
  • Breakage and instability of chromosomes resulting from inadequate telomere maintenance may lead to genetic changes that allow cells to divide in an uncontrolled way, resulting in the development of cancer in some people with dyskeratosis congenita. (
  • Metaphase I. pairs of homologous chromosomes move to the equator of the cell. (
  • The chromosomes line up across the center of the cell. (
  • Metaphase is a stage in the cell cycle where all the genetic material is condensing into chromosomes . (
  • During this stage, the nucleus disappears and the chromosomes appear in the cytoplasm of the cell. (
  • Control dividing cells separate their duplicated chromosomes normally to the two daughter cells (left, blue arrows) as compared to cells expressing a mutated form of Cdt1 that is defective in binding to microtubules and exhibit severe delays in accomplishing this task (right, yellow arrows). (
  • During mitosis, microtubules pull the replicated chromosomes into two separate strands, one for each daughter cell. (
  • However, cell division involving amitosis causes an unequal distribution of chromosomes, or may even lead to abnormalities in reproduction and metabolism. (
  • Chromosomes are pulled to opposite ends of the cell. (
  • It results in equal distribution of chromosomes to daughter cells. (
  • The Retinoblastoma protein (RB) and DREAM complex (DP, RB-like p130, repressor E2F4/5, and MuvB) are transcriptional repressors that inhibit the expression of both the early G1/S and late G2/M cell cycle genes during G0 or the quiescent phase of the cell cycle. (
  • We observed that DREAM and RB cooperate to repress cell cycle genes during G0 and early G1. (
  • When activated by DNA damage, the tumor suppressor p53 protein contributes to reducing the levels of all cell cycle dependent genes. (
  • DREAM and RB cooperatively repressed G1/S cell cycle genes after p53 activation. (
  • In contrast, p130 and the related p107 protein contributed to repression of the late G2/M cell cycle genes after p53 activation and during a normal cell cycle. (
  • The p53 tumor suppressor is a mammalian transcription factor which controls the genes that stop the cell cycle, repair DNA, and even trigger cell death in response to DNA damage ( Kastenhuber and Lowe, 2017 ). (
  • Many cell cycle and DNA repair genes are conserved between vertebrates and plants, yet a p53 ortholog has never been found in any plant genome sequence. (
  • iii ) genes that trigger a cell death program (for when damage is too severe). (
  • The E2F transcription factors have been shown to be critical for the temporal expression of the oscillating cell cycle genes.This review will focus on how the oscillation of E2Fs and their targets is regulated by transcriptional, post-transcriptional and post-translational mechanism in mammals, yeast, flies, and worms. (
  • We demonstrate that these two phenomena are independent of one another, with viral early genes being responsible for cell cycle inhibition, and post-replicative viral gene(s) responsible for the cell cycle shift. (
  • The prolonged S-phase upregulation of genes from clusters of signal transduction, DNA damage repair, stress response, cell cycle and energy generation and down-regulation of genes from Unfolded Protein Response (UPR) pathways were observed in stress-dose irradiated cells when studied with the microarray technique. (
  • Early deletion of Smo results in an increased RGC and photoreceptor cell production, which is accompanied by altered expression of key bHLH proneural genes. (
  • Interestingly, the expression of both THAP9 and THAP9-AS1 exhibit a striking periodicity throughout the S-phase, reminiscent of cell cycle regulated genes. (
  • The cell cycle genes controlling the G1/S phase transition were detected by immunohistochemistry, westernblot and RT-PCR. (
  • Our previous study revealed that angiogenic genes were elevated in LNCaP-MST (MDM2 transfected cells) compared to LNCaP. (
  • During this phase, the cell is able to synthesise various genes that are needed later on in the cell's life cycle. (
  • By using cardiomyocyte-specific inducible gain (GOF) and loss (LOF) of function models of the canonical WNT pathway, the authors found that WNT/β-Catenin signaling governs the expression of cell cycle and oxidative phosphorylation-related genes in adult cardiomyocytes. (
  • Enhanced β-Catenin transcriptional activity in the GOF model resulted in increased expression of cell cycle re-entry and cytokinesis genes, while a decrease in the transcriptional activity of β-Catenin in the LOF model led to a modest increase of genes related to oxidative phosphorylation. (
  • [1] [2] The function of TFs is to regulate-turn on and off-genes in order to make sure that they are expressed in the desired cells at the right time and in the right amount throughout the life of the cell and the organism. (
  • We use 'conserved' and 'cycling' genes by Lu et al. (
  • Genes controlling hyphal development include ones that are upregulated during cell elongation and adherence to epithelia. (
  • These cycles are set by circadian clock genes that are found in nearly every cell in our bodies. (
  • We determined that Cyclin D-CDK4 phosphorylation of p130 contributes to disruption of the DREAM complex during cell cycle entry from G0. (
  • Cell cycle-dependent phosphorylation and regulation of cellular differentiation. (
  • Here, we focus on a direct mechanistic link involving phosphorylation of differentiation-associated transcription factors by cell cycle-associated Cyclin-dependent kinases. (
  • Fascaplysin will prove to be a useful tool in studying the consequence of Cdk4 inhibition, especially in cells containing inactivated p16, and caused G1 arrest and prevented pRb phosphorylation at sites implicated as being specific for Cdk 4 kinase. (
  • For a short window on hyphal induction, far before START in the cell cycle, the phosphorylation profile is transformed before reverting to the yeast profile. (
  • This effect is abolished when Ser-277 is replaced with alanine suggesting the phosphorylation of Ser-277 plays an important role in cell cycle regulation. (
  • Furthermore, a direct inhibition of Rad3-induced phosphorylation of Cds1 or Chk1 in cells exposed to genotoxins has not been demonstrated (Moser (Calvo (Moser deletion on Cdc25 stability in has not been previously reported. (
  • Its genetic amenability continues to make it a favorite model to decipher the principles of how changes in cyclin-Cdk activity translate into the intricate sequence of substrate phosphorylation events that govern the cell cycle. (
  • ATR kinase exerts its function in genome maintenance by focusing on and phosphorylating the key effector kinase CHK1, which mediates cell cycle arrest through the phosphorylation and degradation of the CDC25 phosphatase (13C15). (
  • The results reveal the central role of protein phosphorylation in the atypical cell cycle regulation of a divergent eukaryote. (
  • Fractionation experiments indicate that p54 interacts, directly or indirectly, with the nuclear lamina, and analysis of p54 in cultured cells suggests that this interaction is controlled by cell cycle-dependent posttranslational modification, most likely phosphorylation. (
  • 2 examine different phases of the cell cycle in the budding yeast Saccharomyces cerevisiae , and their findings converge on the same answer: positive feedback. (
  • To this end, we test the hypothesis that localized translation of a single cell cycle regulator (cyclin) is a way for budding yeast cells to determine when the daughter cell is ready for independent life. (
  • The budding yeast S. cerevisiae was one of the pioneering model organisms to study the cell cycle. (
  • Integrative analysis of cell cycle control in budding yeast. (
  • The cell cycle in mammalian cells is regulated by a series of cyclins and cyclin-dependent kinases (CDKs). (
  • The connections between cell cycle exit and terminal differentiation remain poorly understood. (
  • The initial aim of this project was to further investigate if the CKI p27Xic1 could promote differentiation in addition to, and independently of, its well characterised cell cycle exit function. (
  • We discovered that p27Xic1 does not affect differentiation during pronephrogenesis, but instead controls pronephric organ size through its cell cycle exit function. (
  • Cell Cycle in Development , Springer Verlag, pp.565-76, 2011, Results and Problems in Cell Differentiation, ⟨10.1007/978-3-642-19065-0_23⟩ . (
  • Dihydroartemisinin inhibits the human erythroid cell differentiation by altering the cell cycle. (
  • The substituent at position C-10 is responsible only for the anti-proliferative effect, since 10-deoxoartemisinin did not reduce cell growth but arrested the differentiation of K562 cells. (
  • The mature vertebrate neural retina consists of six major types of neuronal and glial cells and is an excellent system for studying neuronal differentiation. (
  • We provide further evidence that in cultured mouse retinal cells recombinant Shh-N similar suppresses RGC differentiation. (
  • These processes are tightly co-ordinated/-regulated with the cell division cycle and cell differentiation, and are when disrupted or perturbed an underlying cause of cancer and developmental disorders. (
  • ID-8 is an inhibitor of DYRK inhibitor that can sustain embryonic stem cell self-renewal and survival without differentiation. (
  • However, the mechanisms by which cells in the direct vicinity trigger wound repair remains a major question in regenerative biology. (
  • Using our expertise in cell biology, we aim at discovering novel essential pathways that regulate equal partitioning of genetic material and cellular organelles during mitosis and re-assembly of nuclear pore complexes after successful completion of cell division. (
  • Cell Cycle Multiple Choice Questions and Answers (MCQ) PDF Download: Quiz, Practice Tests & Problems with Answer Key covers 9th grade biology solved MCQs. (
  • Biology Test: Ch. The cell undergoes different processes when it has duplicated and as the processes differ, so do the results. (
  • Download latest MCQ questions with answers for Biology Cell Cycle in pdf free or read online in online reader free. (
  • Our cross-functional approaches include different molecular and imaging techniques and are conducted in collaboration with regional and international experts in cell, cancer and developmental disorder biology. (
  • These findings could inform more effective cancer treatments and help answer larger questions about molecular mechanisms, according to Dileep Varma, PhD , assistant professor of Cell and Molecular Biology and senior author of the study. (
  • Dileep Varma, PhD, assistant professor of Cell and Molecular Biology, was the senior author of a study published in the Journal of Cell Biology. (
  • Class 11 Biology Notes for Cell Cycle and Cell Division - Get here the Notes, Question & Practice Paper of Class 11 Biology for topic Cell Cycle and Cell Division. (
  • Below we provided the link to access the Notes, Important Question & Practice Paper of Class 11 Biology for topic Cell Cycle and Cell Division. (
  • So, go ahead and check the Important Question & Practice Paper for Class 11 Biology Notes for Cell Cycle and Cell Division from the link given below in this article. (
  • Cell biology research seeks to understand all aspects of cell growth, survival, and death in the contexts of both health and disease. (
  • Cell Signaling Technology (CST) provides a diverse and comprehensive catalog of rigorously tested and validated products to generate robust and reliable data and support your research into all aspects of cell biology. (
  • Understanding the mechanisms that cause cell death is a critical aspect of cell biology, as many diseases involve aberrant regulation of cell death mechanisms. (
  • The Journal of cell biology, Vol. 114, H. 3. (
  • Eukaryotic cell cycle is a highly ordered process controlled by cyclin-dependent kinases (CDKs) and their corresponding cyclins. (
  • The eukaryotic cell cycle is divided into 5 different phases. (
  • As you can see, the eukaryotic cell cycle has several phases. (
  • 1) Differentiate between the G1, G2, and S phases of the eukaryotic cell cycle. (
  • In our research team we aim to address this topic on basis of the identification of a unique and novel plant regulator that is instantly induced by wounded cells and that plays an essential role in the replenishment of damaged stem cells, being a transcription factor nominated ERF115. (
  • histone cell cycle regulator (hira) gene expres. (
  • So far, SOG1 appears to be the master regulator, delegating downstream responses among various regulators ( Figure 1 ), with ANAC044 and ANAC085 stopping the cell cycle before division. (
  • These findings provided the first clues that the E2F transcription factor might be an important regulator of the cell cycle. (
  • The observation that cyclin-CDK is rate-limiting for mitotic events suggests that increasing the level of this key cell cycle regulator above its endogenous range should accelerate Mitosis, and I show evidence that this is the case. (
  • Together, this work underscores the central role of the mitotic cyclin-CDK regulator, which controls not only the relative timing of individual cell cycle events, but also the growth rate of the cell, and the overall frequency of the cell cycle oscillator. (
  • We identified the uhrf1 gene, a cell cycle regulator and transcriptional activator of top2a expression, as required for hepatic outgrowth and embryonic survival. (
  • Flow cytometry , immunofluorescence or immunohistochemistry can be used to easily determine the cell cycle status. (
  • Using flow cytometry, immunofluorescence or immunohistochemistry, researchers can quickly and accurately determine the cell cycle status or tissue localization of individual cells within proliferating populations. (
  • The samples are subsequently analyzed using flow cytometry to assess ploidy, identify abnormal DNA stemlines, and estimate the DNA index (DI) and cell cycle phase distributions of stemlines. (
  • We tested this hypothesis in eight immortalized cell lines by correlating immunocytofluorescent labeling of VGSCs or Na + ,K + -ATPase, with propidium iodide or DAPI fluorescence using flow cytometry. (
  • Further, flow cytometry revealed that FCP significantly increased the sub‑G1 (apoptotic cell population) and G2/M phase population, and the total number of apoptotic cells, in a dose‑dependent manner. (
  • To investigate the mechanism of THU-induced cell growth inhibition, cell cycle analysis using flow cytometry was performed. (
  • Xploid™ is a unique software package for the automated analysis of cell cycle by high throughput flow cytometry. (
  • In addition, sensitivity to CDK4 inhibition was dependent on RB and an intact DREAM complex in both normal cells as well as palbociclib-sensitive cancer cell lines. (
  • ALS concentration-dependently induced autophagy in PANC-1 and BxPC-3 cells, which may be attributed to the inhibition of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR), p38 mitogen-activated protein kinase (p38 MAPK), and extracellular signal-regulated kinases 1 and 2 (Erk1/2) but activation of 5'-AMP-dependent kinase signaling pathways. (
  • It is indicated that p21-mediated inhibition of cdk2 contributes to the cell cycle arrest imposed by p16 and is a potential point of cooperation between the p16/pRB and p14ARF/p53 tumor suppressor pathways. (
  • Here, myosin-II inhibition rescues rupture and partially rescues the DNA damage marker γH2AX, but an apparent delay in cell cycle is unaffected. (
  • Further, inhibition of ERK signaling with a MEK inhibitor (PD0325901) reduced the migration speed of some, but not all satellite cells, indicating that ERK signaling is only required for the migration of a subpopulation of cells. (
  • MDMX inhibition reduced angiogenesis through lowering VEGF levels and induced cell cycle arrest through p21 elevation. (
  • Despite extensive studies on the biochemical mechanism of action, cell cycle perturbations induced by dFdC have not yet been thoroughly investigated, apart from the expected inhibition of DNA synthesis. (
  • Anti-proliferative effects were observed upon treatment of these double-mutant cell lines with the drug combination, and tumor growth inhibition was observed in double-mutant human tumor xenografts, though effects were variable within this subset. (
  • While the inhibition LR-90 of ATR activity prospects to moderate cytotoxicity in normal cells due. (
  • The PUUV strain Kazan wild type (PUUV Kazan-wt) ( 7 , 8 ) was used for subcutaneous inoculation of bank voles, and Vero E6 cell line-adapted PUUV strain Kazan (PUUV Kazan-E6) ( 7 ) was used in inhibition experiments and as a positive control in the real-time RT-PCR. (
  • Cell-cycle development is monitored by checkpoint pathways that pause the cell routine when tension arises to threaten the integrity from the genome. (
  • We discovered that checkpoint-defective alleles suppress the MMS awareness as well as the checkpoint recovery defect of cells. (
  • Furthermore induced degradation of checkpoint-functional Mrc1 rescues the checkpoint recovery defect of cells partially. (
  • The G1 checkpoint determines whether all conditions are favorable for cell division to proceed. (
  • The G1 checkpoint, also called the restriction point (in yeast), is a point at which the cell commits to the cell division process. (
  • External influences, such as growth factors, play a large role in carrying the cell past the G1 checkpoint. (
  • In addition to adequate reserves and cell size, there is a check for genomic DNA damage at the G1 checkpoint. (
  • We are studying which factors in the cell are responsible for recognizing damage in distinct stages of the cell cycle, and how they start the checkpoint pathway by activation of the kinase activity of Mec1/ATR, the initiating protein kinase in this signal transduction pathway. (
  • A checkpoint is basically a stop in the cell cycle where the cell is examined for internal and external signals which in turn decides whether the cell will continue dividing or not. (
  • Just like how a student has to pass an exam to get promoted to the next semester, a cell has to pass the checkpoint to get promoted to the next phase. (
  • The only difference being that the student needs to get 34/100 to pass the exam whereas the cell needs to get 100/100 to pass the checkpoint. (
  • Towards the end of the G2 Phase comes the G2 Checkpoint to check if the cell is ready to transition to the M Phase. (
  • The metaphase checkpoint is an important checkpoint that ensures that the cell is ready to divide. (
  • The G 1 checkpoint determines whether all conditions are favorable for cell division to proceed. (
  • The G 1 checkpoint, also called the restriction point (in yeast), is a point at which the cell irreversibly commits to the cell division process. (
  • External influences, such as growth factors, play a large role in carrying the cell past the G 1 checkpoint. (
  • In addition to adequate reserves and cell size, there is a check for genomic DNA damage at the G 1 checkpoint. (
  • As at the G 1 checkpoint, cell size and protein reserves are assessed. (
  • A checkpoint called, Restriction point determines whether a cell continues its journey of cell cycle, dies or enters into G0 phase. (
  • In the present review, we illustrate the essential features of checkpoint controlled and uncontrolled cell-cycle oscillations by using mechanical metaphors. (
  • The checkpoint-controlled cell cycles are always driven by a negative-feedback loop amplified by double-negative feedbacks (antagonism). (
  • In addition to this competent complex, at least two cell cycle regulated protein kinase pathways are required to affect a transition to a post-replicative chromosomal state. (
  • These findings show that ALS induces cell cycle arrest and promotes autophagic cell death but inhibits EMT in pancreatic cancer cells with the involvement of PI3K/Akt/mTOR, p38 MAPK, Erk1/2, and Sirt1-mediated signaling pathways. (
  • Neuronal precursor cells in the developing cerebellum require activity of the sonic hedgehog (Shh) and phosphoinositide-3-kinase (PI3K) pathways for growth and survival. (
  • Cells have thus evolved molecular signalling pathways that sense DNA damage or environmental stress and activate cell cycle checkpoints. (
  • However, questions remain about the spatiotemporal control of satellite cell behavior during regeneration, and to what extent different signaling pathways contribute to each step. (
  • Understand the Cell Cycle, how cells signal with each other (cell signaling pathways), and how problems with these processes can result in diseases such as cancer, asthma, idiopathic pulmonary fibrosis, COPD, and many others in this medical course. (
  • Cells respond to a multitude of signals in the extracellular environment, often by activating intracellular signaling pathways that elicit changes in cell function or behavior. (
  • Correct regulation of the cell cycle is of crucial importance during the development of all multi-cellular organisms. (
  • During this process, not only the genetic material but also the cellular organelles have to be equally distributed to the newborn cells to allow for their proper functioning. (
  • During the cell cycle phases, DNA levels change, facilitating the use of DNA dyes such as 7-AAD to generate characteristic cellular DNA content profiles (see the figure below). (
  • p27Xic1 has been shown to be involved in cell fate determination during gliogenesis, neurogenesis, myogenesis and cardiogenesis and many mammalian Cip/ Kip CKI homologues of p27Xic1 have been described as important regulators of cellular processes beyond control of cell division. (
  • However, functions of APC in other important cellular processes, such as cell cycle control or aneuploidy, are only beginning to be studied. (
  • However, cells with a mutated topo IIα isoform and lacking topo IIβ did not arrest, suggesting that the cellular consequence of M2- or M3-APC expression depends on functional topoisomerase II. (
  • The different cell types were compared for their morphological features and clarity of cellular detail under all four stains. (
  • Following treatment of DU145 human prostate cancer cells with 10, 25 and 50 mg ml 1 of WCE, respectively for 6 h, WCE significantly decreased the cellular viability of DU145 cells. (
  • The determination of cellular response to a variety of drugs and biological stimulations is one of the trending elements prevailing in the global cell cycle analysis market. (
  • This dissertation presents a collection of mathematical models for cellular response to the most common forms of anti-cancer therapy (radiation and chemotherapy) and the role of the cell cycle in this response. (
  • and combination therapy with newer agents that target the cell cycle or cellular metabolism. (
  • The cellular pharmacodynamic models are based on the key concept of "cellular damage" that results from exposure to therapy and has distinct kinetics from cell kill. (
  • Finally, a first step is taken towards allowing for microenvironmental input into cellular response, by developing a model for the cell cycle that is driven by metabolic inputs and external growth factors. (
  • This is the multihit theory of tumorigenesis, in which a series of multiple triggering events in the genetic and cellular makeup of a cell ultimately cause cancer. (
  • Cell cycle is a strictly regulated phenomenon that involves duplication and division of cellular material between daughter cells. (
  • The first documented details of cellular division can be found in the discovery of cell division by a 19th century professor. (
  • Finally, G2 phase involves further cell growth and organisation of cellular contents. (
  • Each step of the cell cycle is closely monitored by external signals and internal controls called checkpoints . (
  • There are three major checkpoints in the cell cycle: one near the end of G1, a second at the G2/M transition, and the third during metaphase. (
  • Cyclins and cyclin-dependent kinases (Cdks) are internal molecular signals that regulate cell transitions through the various checkpoints. (
  • To prevent a compromised cell from continuing to divide, there are internal control mechanisms that operate at three main cell cycle checkpoints. (
  • Figure 10.11 The cell cycle is controlled at three checkpoints. (
  • This process of maintaining the standards occur through Cell Cycle Checkpoints and Cell Cycle Regulators. (
  • It was Leland H. Hartwell who discovered the role of checkpoints while experimenting on yeast cells. (
  • For the sake of understanding, Cell Cycle Checkpoints can be considered as the equivalent of exams for a student. (
  • The cell cycle can be halted at 3 different checkpoints. (
  • The cell cycle is controlled at three checkpoints. (
  • In many plant species, exit from the division cycle is accompanied by the onset of endoreplication representing a modified version of the normal mitotic cell cycle during which DNA is replicated without mitosis. (
  • Our analyses show that Hh signaling is critical in proliferating retinal progenitor cells prior to their withdrawal from the final mitotic cell cycle. (
  • The nucleus of the cell is clearly stained and appears to have tiny dots and one or more dark nucleoli inside. (
  • These videos and activities will walk them through each stage, describing what is happening to the cell and the nucleus. (
  • The dynamical system encompasses the relative motion of the nucleus to the cell membrane and a state variable measuring the extent of damage to the cytoskeleton. (
  • During the normal cell cycle, Cdc25 localizes predominantly in the nucleus from late G2 until the onset of mitosis. (
  • We detected phosphorylated tau protein as small dense dots in the cell nucleus, which strongly colocalize with intranuclear speckle structures that were also labelled with an antibody to SC35, a protein involved in nuclear RNA splicing. (
  • c. more DNA in its nucleus than the parent cell. (
  • Hooke discovered the nucleus of the cell. (
  • The process that separates duplicated genetic material carried in the nucleus of a parent cell into two identical daughter cells is called Metaphase. (
  • The partition of a cell's nucleus into daughter cells is called Karyokinesis. (
  • Additionally, the nucleus of the cancer cell appears larger and darker than the ones in normal cells. (
  • We ll take a look at why eukaryotic cells require mitotic division, and then explore the details of the cell cycle and its regulation, specifically the mechanics of mitosis and cytokinesis. (
  • The last stage of the cell cycle is cytokinesis, or the division of the cytoplasm. (
  • Cytokinesis -Division of the cytoplasm following mitosis caused by the cell membrane pinching inwards until the cell splits into two. (
  • Cell Plate -A segment of new cell wall that grows in plant cells during cytokinesis. (
  • Cytokinesis is the final physical cell division that follows telophase, and is therefore sometimes considered a sixth phase of mitosis. (
  • Additional studies, including S-phase and cytokinesis makers, would help clarify the effect of GOF on cardiomyocyte cell cycle. (
  • The shortest phase of the cell cycle is cytokinesis because all the previous stages help prepare the cell to divide, so all the cell has to do is divide and nothing else. (
  • Definition - The phase of the cell cycle that includes mitosis and cytokinesis. (
  • In plants cytokinesis takes place by cell plate formation which is laid down at the middle and then grows to the sides. (
  • The order of cytokinesis and karyokinesis varies from cell to cell. (
  • In mitosis first karyokinesis takes place and after this cytokinesis occurs resulting in the formation of two daughter cells. (
  • In eukaryotes, cyclin-cyclin-dependent kinase (cyclin-Cdk) complexes act as master regulators of the cell division cycle by phosphorylating numerous substrates. (
  • In this study, we examined the relationship between TRIB2 and cell division cycle 25 (CDC25) family of dual-specificity protein phosphatases (mammalian homologues of Drosophila String), which are key physiological cell cycle regulators. (
  • Tumor predisposition in an individual with chromosomal rearrangements of 1q31.2-q41 encompassing cell division cycle protein 73. (
  • More recently, microarray data have shown that many OTU family members were rapidly up-regulated or down-regulated in human esophageal epithelial cells and lymphocytes when stimulated by different cytokines, such as ovarian tumor domain containing 6B (OTUD-6B), a novel DUB of the OTU family members. (
  • Several studies have revealed that exposure to ionizing irradiation (IR) may lead to increased accumulation of tumor-infiltrating T regulatory cells (Tregs), which in turn promotes tumor resistance to radiation therapy. (
  • The method of oncotripsy (from Greek, onco- meaning "tumor" and -tripsy "to break") exploits aberrations in the material properties and morphology of cancerous cells to target them selectively using tuned low-intensity pulsed ultrasound. (
  • SU6668 is a cell-permeable indolinone compound that acts as a potent ATP-competitive inhibitor against RTKs (receptor tyrosine kinases) Kit, PDGFR, VEGFR2 (Flk-1KDR), FGFR1 activity in vitro (IC50 0.01, 0.1, 3.9, and 3.8 M, respectively) and PDGFVEGFbFGF-mediated angiogenesis and tumor development. (
  • A tumor is a ball of quickly dividing cells that can form from a single cancerous cell. (
  • Tumor -Mass of cells formed from a quickly dividing cancer cell. (
  • For example, in addition to promoting sleep, melatonin can also stop tumor growth and protect against the spread of cancer cells. (
  • The Cell Cycle Assay is a high content imaging assay that reports the distribution of a cell population among G1, S, G2, and M phases of the cell cycle. (
  • C) A scatterplot of cells showing the EdU and DAPI labeling intensities of cell sub-populations in different phases of the cell cycle. (
  • Results indicated a general regulation of critical cell cycle components, in addition to the possible regulation by signaling cascades (Akt/GSK-3β and ATR/Chk2) that are known to regulate G1/G0 phases of the cell cycle. (
  • According to Varma, cancer drugs targeting CDT1 could improve on current therapies because CDT1 is active in two separate phases of the cell cycle. (
  • The g1 phase, Gap 1 phase, or Growth 1 phase, is the first of four phases of the cell cycle that takes place in eukaryotic cell division. (
  • Our results highlight the role of m 6 A in regulating cyclin D1 mRNA stability and add another layer of complexity to cell-cycle regulation. (
  • ALS remarkably arrested PANC-1 and BxPC-3 cells in G 2 /M phase via regulating the expression of cyclin-dependent kinases 1 and 2, cyclin B1, cyclin D1, p21 Waf1/Cip1, p27 Kip1, and p53. (
  • Role of cell cycle control and cyclin-dependent kinases in breast cancer. (
  • Immunoblotting demonstrated a dose‑dependent downregulation of cyclin B1, cyclin‑dependent kinase 1, cell division cycle 25c, pro‑caspases ‑3, ‑6, ‑8 and ‑9, and poly (adenosine diphosphate‑ribose) polymerase (PARP) in FCP‑treated A549 cells. (
  • Here, an effort was made to enhance TK/prodrug efficacy by coexpression of a cyclin-dependent kinase inhibitor (CKI), p27, to render cells resistant to TK/prodrug by inhibiting DNA synthesis. (
  • Restriction point control of the mammalian cell cycle via the cyclin E/Cdk2:p27 complex. (
  • Dive into the research topics of 'Restriction point control of the mammalian cell cycle via the cyclin E/Cdk2:p27 complex. (
  • a Western blots and densitometry analysis showing changes in the expression of cell cycle markers, such as p21 cip , p18 and cyclin D1 upon the over expression of ERRβ in MCF7 cells. (
  • I-L ) Cyclin E + /GFAP + cells were broadly observed in the spared tissue (insert in L). ( M-P ) E2F5 is not only expressed by GFAP + hypertrophic astrocytes (insert in P) in the lesion scar border, but also in the central lesion area where GFAP + astrocytes are absent. (
  • The cell cycle machinery of Saccharomyces cerevisiae consists of a central negative feedback oscillator comprising cyclin-CDK and its antagonist, APCCdc20. (
  • Either by directly triggering events, or by entraining independent oscillators controlling events, the cyclin-CDK oscillator regulates the key events of the cell cycle. (
  • Quite surprisingly, this increase in cyclin-CDK abundance also accelerates the frequency of the cell cycle oscillator as a whole through its effect on growth. (
  • CDKs -"Cyclin-dependent kinases" coordinate with cyclins to control the cell cycle. (
  • In the end, Sir Paul Maxime Nurse discovered the role of CDK's (Cyclin-Dependant Kinase's) while experimenting on yeast cells. (
  • In exfoliative vaginal cytology, epithelial cells undergo constant growth, shedding and replacement. (
  • The cell cycle consists of four main phases: G1, S, G2, and M. Most cells undergo these cycles up to 40-60 times in their life. (
  • Mitosis - All unicellular or Single-celled organisms including bacteria and algae, which reproduce asexually undergo mitosis process of cell division. (
  • Meiosis - All multicellular organisms including plants, animals, birds, and insects which reproduce sexually undergo meiosis process of cell division to create their reproductive cells. (
  • Many cells undergo symmetry-breaking polarization toward a randomly oriented "front" in the absence of spatial cues. (
  • All active eukaryotic cells undergo this cycle as they grow and divide. (
  • Lack of nutrition, lack of growth factors, and the inability of the cells to undergo metabolic changes are few of the reasons for cells to get arrested in G1 phase. (
  • Anticipated to undergo 3 cycles of chemotherapy (solid tumour cancer participants) OR autologous stem cell transplantation (haematological cancers - HSCT participants). (
  • Damage on the cells develops in the order of millions of ultrasound cycles, and the failure mechanism is explained as a fatigue process. (
  • The present study was conducted to elucidate the anti‑cancer effect and molecular mechanism of flavonoids from Citrus platymamma (FCP) on A549 cells. (
  • In this review, we propose a mechanism for neuronal cell cycle reentry and the development of AD. (
  • In this study, we found that THU has an alternative mechanism for inhibiting cell growth which is independent of CDA expression. (
  • Each mechanism of cell kill, each agent in combination therapy, and each cycle in fractionated therapy increases the damage function (the "additive damage" model). (
  • To investigate the effect of HBV on the proliferative ability of host cells and explore the potential mechanism. (
  • Previous data show that the kinetochores are clustered together during most of the cell cycle, but the mechanism and the biological significance of kinetochore clustering are unknown. (
  • This study also identified a phase-specific cell cycle arrest mechanism involving the Rb/E2F DNA-binding complex in both anoxic liver and kidney tissues. (
  • The fungal cell cyle is considered with respect to the mechanism of sequential gene expression in Candida albicans, since little is known about the cell cycle in pathogenic molds. (
  • Additionally, from the PubMed Database, we found that only several articles in regard to the effects of DHM on melanoma have been reported in the past two decades, and those reports only showed DHM-inhibited migration, invasion and adhesion of mouse melanoma B16 cells in vitro , and decreased pulmonary metastasis of B16 cells in mice ( 19 - 21 ). (
  • Conclusions/Significance Together, our data establish that the 20-amino acid repeat region of APC interacts with topo IIα to enhance its activity in vitro, and leads to G2 cell cycle accumulation and aneuploidy when expressed in cells containing full-length APC. (
  • Background Fish oil supplementation has been shown to alter gene expression of mononuclear cells both in vitro and in vivo. (
  • Here, we describe the effects of whole cranberry extract (WCE) on the behaviour of DU145 human prostate cancer cells in vitro. (
  • These findings demonstrate that phytochemical extracts from the American cranberry (Vaccinium macrocarpon) can affect the behaviour of human prostate cancer cells in vitro and further support the potential health benefits associated with cranberries. (
  • An image depicting head and neck squamous cell carcinoma in vitro can be seen below. (
  • Head and neck squamous cell carcinoma in vitro (cell culture). (
  • In vivo regeneration studies enable a snapshot assessment of cell behavior, whereas in vitro cultures allow for time-lapse analysis but cannot fully recapitulate the complex multicellular, biochemical and biophysical interactions that occur in the native environment. (
  • We used SH-SY5Y human neuroblastoma cells as an in vitro model to further study the functions of tau protein. (
  • Ovarian cancer cells growing in vitro were treated with dFdC for I hr in a range of concentrations from 10 nM to 10 pM. (
  • When fast-dividing mammalian cells are grown in culture (outside the body under optimal growing conditions), the length of the cycle is about 24 hours. (
  • We shall review our knowledge of the mechanisms which coordinate activation of the kinase with cell cycle-specific events in mammalian cells. (
  • Cells that have temporarily or reversibly stopped dividing are said to have entered a state of quiescence called G0 phase. (
  • G0 is a resting phase where the cell has left the cycle and has stopped dividing. (
  • The cell cycle starts with this phase. (
  • Some cells enter the G0 phase semi-permanently and are considered post-mitotic, e.g., some liver, kidney, and stomach cells. (
  • During this phase, the biosynthetic activities of the cell, which are considerably slowed down during M phase, resume at a high rate. (
  • Correct execution of cell division requires duplication of all genetic material during S-phase followed by its precise partitioning between two daughter cells during mitosis. (
  • Finally, in the G2 phase, cells continue to grow and prepare for mitosis. (
  • Micronuclei (MN) formation is generally attributed to error in DNA synthesis or mitosis, which are represented by the S or G(2)/M phase respectively, in the cell-cycle histogram. (
  • We propose a model where Dia2 mediates Mrc1 degradation to greatly help cells job application the cell routine during recovery from MMS-induced DNA harm in S-phase. (
  • This shift is associated with an increase in the geminin/Ki67 ratio, signifying a shortening of G1 phase in breast cancer cells. (
  • WCE also decreased the proportion of cells in the G2-M phase of the cell cycle and increased the proportion of cells in the G1 phase of the cell cycle following treatment of cells with 25 and 50 mg ml 1 treatment of WCE for 6 h. (
  • There is also variation in the time that a cell spends in each phase of the cell cycle. (
  • In rapidly dividing human cells with a 24-hour cell cycle, the G1 phase lasts approximately nine hours, the S phase lasts 10 hours, the G2 phase lasts about four and one-half hours, and the M phase lasts approximately one-half hour. (
  • Moving forward from this initiation point, every parameter required during each cell cycle phase must be met or the cycle cannot progress. (
  • A cell that does not meet all the requirements will not be allowed to progress into the S phase. (
  • In stationary phase yeast cells 2D gel electrophoresis shows that there is a diverse pool of Fkh2 phospho-isoforms. (
  • This transformation does not occur when stationary phase cells are reinoculated into fresh medium supporting yeast growth. (
  • ii) the alteration of S phase of cell cycle and (iii) the induction of programmed cell death of early erythroblasts in a dose dependent manner within 24h. (
  • In the S-phase of the cell cycle, THAP9 expression exhibits stress-specific effects ranging from moderate enhancement to no change. (
  • miR-6883 Family miRNAs Target CDK4/6 to Induce G1 Phase Cell-Cycle Arrest in Colon Cancer Cells" 2017, Cancer Res. (
  • For 30 minutes prior to fixation, cells are incubated with EdU, a thymidine analog, which is taken into cells and incorporated into the DNA of those that are replicating their genome as part of S-phase. (
  • Cells are then fixed, and the EdU in S-phase cells is labeled using click chemistry. (
  • What is G1 phase of cell cycle? (
  • Role of the UBL-UBA protein KPC2 in degradation of p27 at G1 phase of the cell cycle. (
  • While moving through the cell cycle, the cells don't transition from one phase to another just simply. (
  • If any of the above issues are encountered, the cell will not move to the next phase of the cycle. (
  • The cell will instead repair itself and then move to the next phase. (
  • If any of the above requirements are not met, the cell will immediately stop the process of division and will not transition to the S Phase. (
  • Mitosis that is cell division's custom is involved by the M phase. (
  • Each phase is utilized to explain what type of change the cell is experiencing. (
  • The second stage of the cell cycle is known as mitosis or M phase. (
  • Cells that have genetic mutations are put in the G 0 phase to make certain that they aren't replicated. (
  • The cell spends most of its time in this phase. (
  • The growth phase of a cell is referred to as the G1 phase. (
  • The G1 phase is when cells are the most active. (
  • Recent experimental evidence has demonstrated the central role of the cdc2 protein kinase in the transition from G2 to M phase in eukaryotic cells. (
  • In rapidly dividing human cells with a 24-hour cell cycle, the G 1 phase lasts approximately nine hours, the S phase lasts 10 hours, the G 2 phase lasts about four and one-half hours, and the M phase lasts approximately one-half hour. (
  • The cell cycle has four sequential phases: G0/G1, S, G2, and M. During a cell's passage through cell cycle, its DNA is duplicated in S (synthesis) phase and distributed equally between two daughter cells in M (mitosis) phase. (
  • They are also used by the cells to monitor internal and external conditions before proceeding with the next phase of cell cycle. (
  • Initially in G1 phase, the cell grows physically and increases the volume of both protein and organelles . (
  • In S phase, the cell copies its DNA to produce two sister chromatids and replicates its nucleosomes. (
  • What is the longest phase in cell cycle? (
  • Towards exploring this discrepancy, the investigators created cells with dysfunctional CDT1, and found that these mutant cells stalled during the mitosis phase and never correctly divided in two. (
  • Of notice, HR-mediated repair occurs preferably during S/G2 phase of the cell cycle since sister chromatids can be used as a template for error-free DNA repair (28C30). (
  • LR-90 As an alternative to HR, cells may repair DSBs using non-homologous end joining (NHEJ), which is usually relatively less favored in S/G2 as compared to in the G1 phase of the cell cycle (30,31). (
  • Here the daughter cells of the previous M phase begin G1 phase. (
  • Normal cell metabolism takes the center stage in this phase. (
  • G1 phase duration is different for different cells. (
  • Terminally differentiated cells or end cells which do not have the capacity to divide any further like neurons and striated muscle cells or voluntary muscle cells are arrested in this G1 phase. (
  • The tumour promoter and protein kinase C agonist, 12-O-tetranodecanoyl-phorbol-13-acetate (TPA), has been reported to show a radiomimetic action because it transiently delays the passage of HeLa cells through the G2 phase, as do ionizing radiation and other DNA damaging agents. (
  • Thus, in the memory phase of immunity, memory helper T cells are maintained in BM as resting but highly reactive cells in survival niches defined by IL-7-expressing stroma cells. (
  • During the two G phases, cell growth, protein synthesis,and enzyme synthesis are occurring, while during the S phase DNA is replicated. (
  • What phase do cells spend the least time in? (
  • G1 is typically the longest phase of the cell cycle. (
  • One significant difference between growth phases is that the first growth phase is about cell growth while G2 is about cell division. (
  • G2 phase is a period of rapid cell growth and protein synthesis during which the cell prepares itself for mitosis. (
  • In the G1 phase, a cell grows rapidly and carries out its routine functions. (
  • G2 phase is where the cell grows again, and prepares for mitosis. (
  • The cell can remain in Quiescent phase for a long time. (
  • The cell cycle goes trough G1 , S, G2 and then mitosis or M phase. (
  • Which Phase lasts for the maximum duration in cell cycle? (
  • What is G0 (quiescent phase) of cell cycle? (
  • G0 or quiescent phase is the stage wherein cells remain metabolically active, but do not proliferate unless called to do so. (
  • 1983 abstract: 'The cell cycle properties of undifferentiated spermatogonia in the Chinese hamster were analysed by the fraction of labelled mitoses technique (FLM) in whole mounted seminiferous tubules. (
  • Article: The effects of low dose 60 Co-gamma-radiation on radioresistance, mutagenesis, gene conversion, cell cycle and transcriptome profile in Saccharomyces cerevisiae Journal: International Journal of Low Radiation (IJLR) 2008 Vol.5 No.4 pp.290 - 309 Abstract: The underlying principles of low (stress)-dose Radiation-Induced Radioresistance (RIR) are inadequately understood. (
  • abstract = "Numerous top-down kinetic models have been constructed to describe the cell cycle. (
  • Many cells do not enter G0 and continue to divide throughout an organism's life, e.g., epithelial cells. (
  • It was up-regulated on human esophageal epithelial cells after interleukin-13 (IL-13) stimulation [17] . (
  • This study aimed to examine the effects of ALS on cell growth, autophagy, and epithelial-to-mesenchymal transition (EMT) and to delineate the possible molecular mechanisms in human pancreatic cancer PANC-1 and BxPC-3 cells. (
  • Epithelial cell cycling predicts p53 responsiveness to gamma-irradiation during post-natal mammary gland development. (
  • In multiple cell types, including mammary epithelial cells, abrogation of p53 (encoded by Trp53) function is associated with increased tumorigenesis. (
  • Methodology/Principal Findings We now demonstrate that the 20-amino acid repeat region of APC (M3-APC) also interacts with topo IIα in colonic epithelial cells. (
  • Throughout the oestrous cycle, the major cells observed are small and large nucleated epithelial cells, anucleated, keratinized epithelial cells and neutrophils. (
  • In humans, the frequency of cell turnover ranges from a few hours in early embryonic development, to an average of two to five days for epithelial cells, and to an entire human lifetime spent in G0 by specialized cells, such as cortical neurons or cardiac muscle cells. (
  • CSPP-L Associates with the Desmosome of Polarized Epithelial Cells and Is Required for Normal Spheroid Formation. (
  • [ 7 ] Similarly, in 2001, Priolo and Laganà reclassified the ectodermal dysplasias into 2 main functional groups: (1) defects in developmental regulation/epithelial-mesenchymal interaction and (2) defects in cytoskeleton maintenance and cell stability. (
  • In turn, as a result of research into the abnormal cancer cell, the basic understanding of the cell has greatly improved. (
  • This, in turn, creates a clonal population of a single abnormal cell. (
  • So I would like to share the 3D modelling clay version, but before we look at the breakage-fusion-bridge cycle, which is an abnormal pattern of chromosome division, we had better look at normal chromosome division (or mitosis). (
  • But when these natural growths of cells become abnormal and start dividing rapidly, it is known as cancer cells. (
  • Why are cancer cells considered abnormal cells? (
  • As this is opposite the usual, the cancer cells are known as abnormal cells. (
  • However, there some cancers such as leukemia and where abnormal cells do not form solid tumors. (
  • Cancer cells often have abnormal shapes, some of them are bigger, and some are smaller than usual. (
  • Moreover, overexpression of ANAC044 only inhibits the cell cycle if the DNA is damaged. (
  • Consistent with previous studies, we show that VACV inhibits and subsequently shifts the host cell cycle. (
  • The microinjection of recombinant GRASP65 without N-terminal myristoylation or a peptide fragment containing Ser-277 into the cytosol of normal rat kidney cells inhibits passage through mitosis. (
  • The results showed that ALS exerted potent cell growth inhibitory, pro-autophagic, and EMT-suppressing effects in PANC-1 and BxPC-3 cells. (
  • A lack of calmodulin results in cell cycle arrest, and a failure in polar growth that accompanies germination of A nidulans spores. (
  • In addition, increased expression of calmodulin in this organism permits growth at suboptimal calcium concentrations, indicating that cell growth is coordinately regulated by calcium and calmodulin. (
  • Effects of DHM treatment on the cell growth of human melanoma SK-MEL-28 cells. (
  • DHM was found to suppress the growth of transplanted tumors derived from human lung cancer GLC-82 cells in nude mice ( 16 ). (
  • cell growth and DNA metabolism, respectively. (
  • The computer implements a controller algorithm to decide when, and for how long, to change the growth medium to synchronise the cell-cycle across the population. (
  • With a secure growth rate, the international cell cycle analysis market is foretold to rise with the help of the support from government and corporate sectors for cell-based researches. (
  • Cytoxicity induced by the herpesvirus thymidine kinase (TK) gene in combination with prodrugs is dependent on cell growth and leads to the elimination of genetically modified cells, thus limiting the duration of expression and efficacy of this treatment in vivo. (
  • An event may be as simple as the death of a nearby cell or as sweeping as the release of growth-promoting hormones, such as human growth hormone (HGH). (
  • Cell cycle-independent phospho-regulation of Fkh2 during hyphal growth regulates Candida albicans pathogenesis. (
  • Cell division is fundamental for the growth and development of organisms, and for the maintenance of tissues and organs throughout life. (
  • On the contrary, cell growth was markedly reduced by DHA, artemisone and artesunate but not by artemisinin, 10-deoxoartemisinin or deoxy-artemisinin. (
  • Convergence of cell cycle regulation and growth factor signals on GRASP65. (
  • The convergence of cell cycle regulation and growth factor signals on GRASP65 Ser-277 suggests that GRASP65 may function as a signal integrator controlling the cell growth. (
  • Cell Growth Differ. (
  • As a result, a combination regimen of THU and gemcitabine might be a more effective therapy than previously believed for pancreatic carcinoma since THU works as a CDA inhibitor, as well as an inhibitor of cell growth in some types of pancreatic carcinoma cells. (
  • Cancer is characterized by uncontrolled growth and division of a cell, with extension beyond the normally limiting basement membrane and through the boundaries of normal cells. (
  • Because of its mutated aggressive genetics, this cell has a selective growth advantage over its neighbors. (
  • 6] These events lead the cancer cell to escape normal cell growth and control mechanisms, to avoid system control mechanisms (ie, immunologic surveillance), and to establish a nutrient supply. (
  • 1. Modeling the cell cycle of S. cerevisiae with special focus on the G1-network to study the interplay of growth and division. (
  • France epub Cell Cycle Control and Plant Development le growth via la ebook Hadopi. (
  • The goal of our study is to understand the effect of MDMX and MDM2, in prostate cancer cells to determine how it regulates cancer growth and metastasis. (
  • This is another period of growth for the cell. (
  • Growth Factors: The cell checks if it is receiving external growth promoting signals to divide. (
  • It's nothing but a portion of the cycle of cell growth and asexual reproduction called the cell cycle. (
  • The growth and division of a single cell into daughter cells is called duplication. (
  • The cell cycle is a repeating series of events that include growth, DNA synthesis, and cell division. (
  • The phases in the reproduction and growth of a cell is known as the cell cycle. (
  • Cell performs normal functions, Cell growth (G1 and g2), Synthesizes new molecules and organelles. (
  • But when the cell growth starts happening without control, and the old ones stay alive instead of dying, cancer occurs. (
  • This extra cell growth causes a mass of tissues known as tumors. (
  • Growth in multicellular cells. (
  • Cancer is the uncontrolled growth and spread of cells. (
  • When conditions are right, cells enter the S stage of the cell cycle and commit to DNA synthesis and replicate their chromosomal DNA. (
  • Combination gene transfer of this CKI with TK therefore sustained the synthesis of TK by genetically modified cells to enhance the susceptibility of bystander cells to prodrug cytotoxicity and increased the efficacy of this gene transfer approach. (
  • DNA synthesis was restored after a G, block of variable, dose-dependent length, but recycling cells were intercepted at the subsequent checlkpoints, resulting in delays in the G,M and G, phases. (
  • The cell cycle is a four stage process, consisting of Gap1, Synthesis, Gap2 and Mitosis. (
  • This is because DNA synthesis requires utmost accuracy and fidelity and the cell is not going to take any risks. (
  • The cell cycle is a 4-stage process consisting of Gap 1 (G1), Synthesis, Gap 2 (G2) and mitosis. (
  • Yeast cells cycle asynchronously with each cell in the population budding at a different time. (
  • Here, we build a cyber-genetic system to achieve long-term synchronisation of the cell population, by interfacing genetically modified yeast cells with a computer by means of microfluidics to dynamically change medium, and a microscope to estimate cell cycle phases of individual cells. (
  • Here we show that Slk19 is required for kinetochore clustering when yeast cells are treated with the microtubule-depolymerizing agent nocodazole. (
  • Previous mathematical modeling suggested that, if more than one cluster were amplified, the clusters would compete for limiting resources and the largest would "win," explaining why yeast cells always make one and only one bud. (
  • Non-proliferative (non-dividing) cells in multicellular eukaryotes generally enter the quiescent G0 state from G1 and may remain quiescent for long periods of time, possibly indefinitely (as is often the case for neurons). (
  • In eukaryotes, the cell cycle is more complicated. (
  • There are 3 different types of cell divisions seen both in eukaryotes and prokaryotes which are: amitosis, mitosis, and meiosis. (
  • Sister chromatids separate from each other and move to opposite poles of the cell. (
  • Because the separation of the sister chromatids during anaphase is an irreversible step, the cycle will not proceed until the kinetochores of each pair of sister chromatids are firmly anchored to at least two spindle fibers arising from opposite poles of the cell. (
  • It forms during the cell cycle so that the sister chromatids (it is a chromosome that is newly copied where two of them are still attached to each other) can be separated to form daughter cells. (
  • One of the molecular mechanisms driving fidelity of cell division is ubiquitylation (or ubiquitination), which is a covalent, posttranslational modification of substrates by a small protein ubiquitin. (
  • 3 Laboratory of Molecular Genetics, Division of Gene Therapy and Hepatology, University of Navarra School of Medicine, Clínica Universitaria and CIMA, Centro de Investigación Biomédica en Red, Pamplona, Spain. (
  • The molecular architecture of fungal walls remains elusive because of difficulty in correlating chemical composition with the ultrastructural layers and uncertainty concerning the linkages connecting major cell wall polymers: glucans, mannan, and chitin. (
  • Stem cells also remain to varying extents in different adult tissues, acting in tissue homeostasis and repair. (
  • Huckins C. The spermatogonial stem cell population in adult rats. (
  • We have reported previously that DHA specifically targets pro-erythroblasts and basophilic erythroblasts, when human CD34+ stem cells are differentiated toward the erythroid lineage, indicating that a window of susceptibility to artemisinins may exist also in human developmental erythropoiesis during pregnancy. (
  • EXPERIMENTAL Methods Animals and transcripts in hematopoietic stem and progenitor cells, Flt3?LSK, Flt3+LSK, and Lin?c-Kit+ cells were sorted on FACSAria, and the total RNA was extracted from sorted cells and reverse-transcribed as described (28, 32). (
  • We show that, in contrast to NDRG2, NDRG4 expression is elevated in GBM and NDRG4 is required for the viability of primary astrocytes, established GBM cell lines, and both CD133(+) (cancer stem cell (CSC)-enriched) and CD133(-) primary GBM xenograft cells. (
  • A major hurdle to studying endogenous stem cell repair is the limitations of standard experimental methods. (
  • Consequently, recent efforts in skeletal muscle research have focused on developing novel ways to visualize endogenous muscle stem cell (satellite cell)-mediated repair. (
  • Stem cells in resting mouse skin can have a cycle period of over 200 hours. (
  • Kirwan M, Dokal I. Dyskeratosis congenita, stem cells and telomeres. (
  • Haematopoeitic stem cell transplant (HSCT) recipients - from day of admission (~day -7) to day +35. (
  • The equator of the cell is called the metaphase plate. (
  • Cell Division Cycle 5-Like Regulates Metaphase-to-Anaphase Transition in Meiotic Oocyte. (
  • Multifaceted animation that shows the different stages of the cell cycle. (
  • To visualize the quantity of DNA which can be found in a cell during the different stages of the cell cycle. (
  • The microscopic evaluation of these cells during exfoliation provides information on the stages of the cycle, possible infections, hormonal status and reproductive defects that might be occurring within the female reproductive system. (
  • For this, they used R26Fucci2aR/Pax7-CreERT2 mice, which express mCherry during G0/G1 and mVenus during S/G2/M stages of the cell cycle in satellite cells. (
  • Cell division is just one of several stages that a cell goes through during its lifetime. (
  • What are the 4 stages of cell cycle? (
  • What happens in the three stages of the cell cycle? (
  • Radiomimetic cell cycle delay induced by tetranodecanoyl phorbol acetate is enhanced by caffeine and by the protein kinase inhibitor 2-aminopurine. (
  • This study investigated the anti-proliferative and apoptotic effect of flavonoids isolated from Korean Citrus aurantium L. using A549 lung cancer cells. (
  • By depleting Hsp90-client oncoproteins, geldanamycin (GA) and 17-allylamino-17-demethoxy-GA (17-AAG) (heat-shock protein-90-active drugs) render certain oncoprotein-addictive cancer cells sensitive to chemotherapy. (
  • These results indicate that DREAM cooperates with RB in repressing E2F-dependent G1/S gene expression and cell cycle entry and supports a role for DREAM as a therapeutic target in cancer. (
  • e Knockdown of CstF-64 or CPSF73 reduced migration of triple negative breast cancer cells. (
  • Triple negative breast cancer cell line MDA-MB-231 was transfected with a control siRNA or an siRNA against CstF-64, CPSF73 or CFIm25. (
  • Microtubule-stabilizing properties of the avocado-derived toxins (+)-(R)-persin and (+)-(R)-tetrahydropersin in cancer cells and activity of related synthetic analogs. (
  • Research has suggested that like cancer, Alzheimer's disease (AD) involves dysfunction in neuronal cell cycle reentry, leading to the development of the two-hit hypothesis of AD. (
  • Moreover, the loss of control of cell proliferations is one of the underlying factors to consider in case of diseases such as cancer. (
  • Errors in the regulation of the cell cycle can cause cancer, which is characterized by uncontrolled cell division. (
  • b , c ERRβ was ectopically expressed in ER + ve breast cancer cells, after 48 h the mRNA levels of p21 cip were examined by RT-PCR and RT-qPCR, p21 cip was significantly up-regulated. (
  • Unlike the small molecule approach where they target CDK4/6 directly, these miRNAs function by silencing the mRNA for production of CDK4/6 thereby reducing the protein levels of CDK 4/6 in cancer cells. (
  • The miRNAs display significant anti-proliferative effects in colorectal cancer, pancreatic cancer and melanoma cell lines. (
  • Errors in this regulation may lead to cell death or genomic instability and consequently to severe diseases such as cancer. (
  • During their visit they were introduced to our Microscopy Facility (Confocal and Wide-field microscopes), carried out cloning experiments and saw how cancer cells are grown. (
  • Final year students of the Experimental High School of the University of Patras visited our lab, carried out cloning experiments and saw how cancer cells are grown and analysed in the Confocal and Time-lapse Microscopes. (
  • In this experiment, a cancer cell line was treated with a dose range of test article for 24 h, and then cell cycle distribution was determined for each sample. (
  • In our study, the cell viability of prostate cancer cell cells (LNCaP) was measured using Trypan blue dye exclusion method after 24, and 48 h of NSC 207895 (NSC) and SJ-172550 (SJ-17) treatment. (
  • The cell could get too many copies of a cancer-promoting gene, or too few copies of a cancer-protecting gene. (
  • Cancer cells divide out of control and have lost the ability to control the cell cycle. (
  • Cancer -Caused by uncontrolled cell division. (
  • Telomerase is also abnormally active in most cancer cells, which grow and divide without control or order. (
  • Traditionally, some types of drugs try to inhibit mitosis in cancer cells, but normally the number of dividing cells in tissue is very small," Varma said. (
  • Increased synergistic activity of the drug combination was identified in colorectal cancer cell lines with concomitant KRAS and PIK3CA mutations. (
  • So how do cancer cells differ from normal cells? (
  • A cancer cell is different than a normal cell in many ways. (
  • By contrast, a cancer cell will keep growing and dividing. (
  • However, researchers have not discovered all of the differences between cancer cells and normal ones. (
  • On the other hand, cancer cells will keep developing until a cluster of cells is formed. (
  • By contrast, cancer cells never interact with each other or receive any command from the brain or other cells. (
  • Cancer cells do none of that. (
  • As the cancer cells do not receive any commands, they keep growing. (
  • In contrast, the cancer cells cannot release this substance and float independently, resulting in infecting other tissues. (
  • But cancer cells travel through your bloodstream or lymph system and reach other organs to affect them. (
  • On the other hand, a cancer cell stays immature and keeps reproducing. (
  • Cancer cells can escape the immune system's detection or release a chemical that prevents the immune cells from coming to the malignant section. (
  • However, cancer cells will always go through Angiogenesis even when it's not necessary at all! (
  • Covalent inhibitors of EGFR family protein kinases induce degradation of human Tribbles 2 (TRIB2) pseudokinase in cancer cells. (
  • L'étude menée en Iraq a utilisé la méthode d'hybridation in situ pour déterminer la fréquence du papillomavirus humain et pour son génotypage dans les échantillons de tissus prélevés auprès de 129 patientes ayant reçu un diagnostic de cancer du sein malin, de 24 patientes porteuses d'une tumeur du sein bénigne et de 20 femmes témoins en bonne santé. (
  • Therefore, LC IR resistance may inform us of the underlying IR resistance mechanisms utilized by other progenitor cells. (
  • These results indicate that Hh signaling is important for RGC and photoreceptor cell fate specification and is required for progenitor cells to maintain the cell cycle. (
  • Endoreplication typically occurs in large, metabolically active, and highly specialized cells, although it can be found as well in cells that do not match this description. (
  • after division, the daughter cells are about half the size of their parent, and they grow before division occurs again. (
  • Transmission between humans occurs by ingestion of faecally contaminated food or water, after which S . Typhi invades the gut mucosa and may be taken up by phagocytic cells, before asymptomatic systemic dissemination to the reticuloendothelial system. (
  • Variation in membrane potential occurs throughout the cell cycle, yet little attention has been devoted to VGSCs and Na + ,K + -ATPase in the cell cycle. (
  • Because it is just one part of the cell cycle, it, on the other hand, occurs. (
  • The process of cell cycle occurs in prokaryotic cells. (
  • Many affected individuals also develop a serious condition called aplastic anemia, also known as bone marrow failure, which occurs when the bone marrow does not produce enough new blood cells. (
  • In single-celled organisms, a single cell-division cycle is how the organism replicates itself. (
  • Cell cycle is a fundamental biological process that ensures organism development and its dysregulation is linked to many human diseases. (
  • Cells multiply to make an organism bigger, to repair damage, or to multiply the number of organisms of that kind. (
  • The developing embryo of any organism is a good tissue to examine for mitosis, since cells must divide at a high rate to transform a fertilized egg (single cell) into the trillions of cells of a viable organism. (
  • The length of the cell cycle is highly variable, even within the cells of a single organism. (
  • The cell division is an important process through which a single-celled develops into a new organism. (
  • E) Binary fission would not allow the organism to have complex cells. (
  • This is done to avoid the passing on of altered genetic material to the daughter cells. (
  • The genetic code for an organisms is contained in the genetic structures in cells. (
  • HIV preferentially infects and replicates in cells expressing the CD4 molecule, the ligand for viral attachment and subsequent cell entry (1). (
  • This process we propose is mediated by the Notch signalling pathway through the establishment of a boundary between these two distinct populations of cells, permitting both compartments to develop in isolation. (
  • Our previous study has found that HepG2.2.15 cell line demonstrated distinct biological features compared with parental HepG2. (
  • They split into two distinct ways to make new cells. (
  • Results Cell cycle, DNA packaging and chromosome organization are biological processes found to be upregulated after intake of fish oil compared to high oleic sunflower oil using a moderated t-test. (
  • mutant cells exhibit delayed kinetochore capture and chromosome bipolar attachment after the disruption of the kinetochore-microtubule interaction by nocodazole, which is likely attributed to defective kinetochore clustering. (
  • This week I was asked to provide a cartoon showing the breakage-fusion-bridge cycle and how it relates to a chromosome abnormality I was describing. (
  • The results in this thesis suggest novel mechanisms by which cell division controls X. laevis segmentation and organ size and how the Notch signalling pathway is able to pattern the pronephros anlagen such that the different compartments of the mature pronephros are able to develop, and thus function. (
  • Although for all organisms it is the goal to divide only if the DNA has been replicated correctly and without damage, years of research have revealed many differences between the ways animals and plants control their cell cycle. (
  • Identifying the underlying mechanisms that control cell division might open opportunities to adjust plant size, yield, and architecture. (
  • In collaboration with the High Throughput Cell-based Screening facility at the IGBMC, we have performed a visual, high-throughput siRNA screen using customized, human 'Ubiquitin Decoders' library and developed multi-parametric control-based gene selection protocols. (
  • Calmodulin and cell cycle control. (
  • In addition to providing an avenue for yeast cell cycle synchronisation, our work shows that control engineering can be used to automatically steer complex biological processes towards desired behaviours similarly to what is currently done with robots and autonomous vehicles. (
  • Little is known about life cycle control of PC. (
  • Krankenhaus-Serie mit Herz epub Cell Cycle Control and Plant Development (Annual Plant Reviews, Humor. (
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  • Cyclins -Chemicals that coordinate with CDKs to control the timing of the cell cycle. (
  • Packed red cells are processed, stored, and shipped to the Division of Environmental Health Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention for analysis. (
  • It's no secret that the regulation of cell cycle is an extremely accurate process and cell cannot afford to make any mistake. (
  • The three of them also shared The Nobel Prize in Physiology or Medicine in 2001 for their pioneering research and discovery in the regulation of cell cycle. (
  • The cell cycle, or cell-division cycle, is the series of events that take place in a cell that cause it to divide into two daughter cells. (
  • The resumption of the mitotic cell division cycle by pheromone-arrested cells that have not mated. (
  • In this project, we formalize biochemical knowledge into a comprehensive mechanistic model of the cell division cycle of baker's yeast, Saccharomyces cerevisiae . (
  • The cell division cycle is the process through which one cell proliferates into two. (
  • I describe work on two major processes in the cell division cycle that reveals two very different modes of regulation. (
  • Positive feedback plays a key role in the ability of signaling molecules to form highly localized clusters in the membrane or cytosol of cells. (
  • During one Kreb's cycle number of carbon dioxide (CO2), molecules released is. (
  • The process involves the migration of two identical DNA molecules to opposite ends of the cell. (
  • In this cycle, DNA (Deoxyribose Nucleic Acid) gets replicated into two daughter DNA molecules and later they are separated. (
  • During G2, the cell has to grow some more and produce any molecules it still needs to divide. (
  • We therefore investigated the gene expression profile in peripheral blood mononuclear cells (PBMCs) after intake of fish oil for 7 weeks using transcriptome analyses. (
  • In the third chapter, we introduce an Empirical Bayes approach to test for periodicity and compare its performance in terms of sensitivity and specificity with that of the other two methods through simulations and by application to the S. Pombe cell-cycle gene expression data. (
  • Otud-6b expression was induced with cytokine stimulation in both mouse Ba/F3 cells and primary B lymphocytes followed a rapid decrease. (
  • BAFF, a B cell-activating factor of the TNF family, could also induce Otud-6b expression on mouse B cells after 4 hours stimulation [18] . (
  • ALS significantly inhibited EMT in PANC-1 and BxPC-3 cells with an increase in the expression of E-cadherin and a decrease in N-cadherin. (
  • In addition, ALS suppressed the expression of sirtuin 1 (Sirt1) and pre-B cell colony-enhancing factor/visfatin in both cell lines with a rise in the level of acetylated p53. (
  • Expression of M3-APC in cells with full-length endogenous APC causes cell accumulation in G2. (
  • More importantly, expression of either M2- or M3-APC also led to increased aneuploidy in cells with full-length endogenous APC but not in cells with truncated endogenous APC that includes the M2-APC region. (
  • In all cases, the results of qRT-PCR confirmed the differences in expression of the selected mRNAs between fibroblasts from the primary culture (C0) and from the first (C1), second (C2), and third (C3) cell passage. (
  • Cell surface expression of VGSCs during phases S through M was double that seen during phases G0 - G1. (
  • The variation in VGSC and Na + ,K + -ATPase expression has implications for both our understanding of sodium's role in controlling the cell cycle and variability of treatments targeted at these components of the Na + handling system. (
  • Figure 1: Schematic of the Cre-lox recombination strategy for satellite cell expression of the ERK FRET biosensor, the experimental set-up used and representative images of ERK activity. (
  • Memory T cells enhance the expression of high-avidity naive B cells. (
  • A cell cycle associated role for TRIB2 is further supported by the cell cycle regulated expression of TRIB2 protein levels. (
  • MTT, colony formation assay and tumourigenicity in nude mice were performed to investigate the effect of HBV on the proliferative capability of host cells. (
  • Results from this assay can detect and elucidate the nature of a proliferative arrest, acceleration, or deviation from the normal cycle. (
  • In this assay, cells grown in microplates are treated with test articles for the desired duration. (
  • The Cell Cycle Assay can be multiplexed with additional measurements, such as cell counts or nuclear morphology, or with immunofluorescent detection of an additional protein of interest. (
  • Jurkat cells were treated without (red) or with 20 µM camptothecin (blue) in a 37 oC, 5% CO2 incubator for about 8 hours, and assayed with Cell Meter™ Fluorimetric Cell Cycle Assay kit. (
  • Jurkat cells were dye-loaded with Cell Meter™ Fluorimetric Cell Cycle Assay kit and RNase A for 30 minutes. (
  • AZ 191 is a potent and selective DYRK1B inhibitor with IC50 of 17 nM in a cell-free assay, about 5- and 110-fold selectivity over DYRK1A and DYRK2, respectively. (
  • The cell cycle, over which cells grow and divide, is a fundamental process of life. (
  • The cell cycle is an ordered series of events by which cells grow and divide to give rise to two daughter cells. (
  • Cells grow and divide as organisms grow and develop. (
  • Cells also grow and divide to repair tissue. (
  • Human cells grow and divide to form new cells whenever our body needs them. (
  • Moreover, SJ-17 reduced the cell viability after 24, 48 h treatment in LNCaP cells. (
  • CST offers a variety of assays and reagents designed to enable evaluations of cell viability and cell death. (
  • Obtain precise data by using one of the many high-quality assays that CST has to offer for efficient, convenient, and cost-effective measurements of cell death and viability. (
  • How does the cell cycle communicate with metabolism? (
  • If true, although the picture is not complete at this stage, it would suggest that WNT signaling might regulate a cardiomyocyte maturation program involving metabolism and cell cycle regulation. (
  • Cells from meiosis result from sexual reproduction. (
  • This last stage is all about prepping the cell for mitosis or meiosis. (
  • Whilst ERK signaling has been shown to regulate both these processes during muscle regeneration, the relationship between cell cycle modulation and migration isn't well characterised. (
  • We propose a model of oncotripsy that follows as an application of cell dynamics, statistical mechanical theory of network elasticity and 'birth-death' kinetics to describe processes of damage and repair of the cytoskeleton. (
  • The problem lies mainly in the sluggish kinetics of the oxygen reduction reaction (ORR) and poor durability of the cathode catalyst, which actually is also the major limiting factor for other energy conversion and storage technologies, such as fuel cells and metal−air batteries. (
  • The aim of our study was to clarify whether cell population kinetics is a vital factor in the cytotoxicity of dFdC in single or repeated treatments and in the dfdC-cisplatin combination. (
  • These results suggest that the kinetics of cell recycling from a first dFdC treatment strongly affects the outcome of a second treatment with either dFdC itself or cisplatin. (
  • Mean SCE/cell was elevated significantly without affecting mitotic index and cell cycle kinetics. (
  • They radiate out to the plasma membrane at the poles in animal cells. (
  • We hypothesized that in addition to doubling DNA and cell membrane in anticipation of cell division, there should be a doubling of VGSCs and Na+,K+-ATPase compared to non-dividing cells. (
  • The opening of VGSCs that allows for the entry of sodium into the cell and depolarization of the cell membrane is required for transition from G0 to G1 [15] The sodium pump returns sodium ions to the extracellular space and restores the resting membrane potential and the intracellular sodium concentration. (
  • In animal cells the cell membrane pinches in half. (
  • The cell membrane. (
  • The cell wall and the secondary cell wall form over this lamella .The cell membrane is internal to the middle lamella. (
  • at the end of mitosis, a neck forms to separate the two daughter cells. (
  • Daughter cells grow in size and prepare for renewed mitosis. (
  • It is essential that the daughter cells produced be exact duplicates of the parent cell. (
  • How many daughter cells are created? (
  • The daughter cells are the result of a single parent cell. (
  • Two daughter cells are the final result from the meiotic process. (
  • Cell division is the process through which the cell duplicates itself to form daughter cells. (
  • By contrast, vaccination with Ty21a was associated with NK cell activity and validated in peripheral blood mononuclear cell stimulation assays confirming superior induction of an NK cell response. (
  • Here, we attempted to identify whether any correlation exists between the cell-cycle effect and MN induction potential using various treatments. (
  • We observed MN induction by all the tested drugs irrespective of their basic effect on cell cycle. (
  • Here, we questioned the contribution of tissue-resident antigen-presenting cells (APCs) to the induction of Tregs upon exposure to IR. (