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 ...
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 ...
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
TY - JOUR. T1 - Linking Cell Cycle to Histone Modifications. T2 - SBF and H2B Monoubiquitination Machinery and Cell-Cycle Regulation of H3K79 Dimethylation. AU - Schulze, Julia M.. AU - Jackson, Jessica. AU - Nakanishi, Shima. AU - Gardner, Jennifer M.. AU - Hentrich, Thomas. AU - Haug, Jeff. AU - Johnston, Mark. AU - Jaspersen, Sue L.. AU - Kobor, Michael S.. AU - Shilatifard, Ali. PY - 2009/9/11. Y1 - 2009/9/11. N2 - To identify regulators involved in determining the differential pattern of H3K79 methylation by Dot1, we screened the entire yeast gene deletion collection by GPS for genes required for normal levels of H3K79 di- but not trimethylation. We identified the cell cycle-regulated SBF protein complex required for H3K79 dimethylation. We also found that H3K79 di- and trimethylation are mutually exclusive, with M/G1 cell cycle-regulated genes significantly enriched for H3K79 dimethylation. Since H3K79 trimethylation requires prior monoubiquitination of H2B, we performed genome-wide ...
Cell cycle variations and DNA aneuploidy, were investigated in different phases of azoxymethane (AOM)-induced colon carcinogenesis in rats by flow cytometry. K-ras gene mutations (transitions Gright curved arrow A) were frequently detected in aberrant crypt foci (ACF) initial pre-neoplastic lesions. The fraction of cells in the G2M-phase of the cell cycle was higher in ACF compared to the normal mucosa of control rats. A similar modification of the cell cycle was found in adenomas and adenocarcinomas but, unexpectedly, also in morphologically normal mucosa from AOM-treated animals indicating that AOM treatment permanently modifies cell cycle control in rat colon mucosa. These alterations, however, were not associated with DNA aneuploidy as reported in human sporadic colorectal cancer, suggesting that tumour development in AOM-treated rats is less dependent on aneuploidy.. ...
Cyclins are key regulators of the cell cycle in all eukaryotes. We have previously isolated two B-type cyclin genes, cycMs1 and cycMs2, from alfalfa that are primarily expressed during the G2-to-M phase transition and are most likely mitotic cyclin genes. Here, we report the isolation of a novel alfalfa cyclin gene, termed cycMs3 (for cyclin Medicago sativa), by selecting for mating type alpha-pheromone-induced cell cycle arrest suppression in yeast. The central region of the predicted amino acid sequence of the cycMs3 gene is most similar to the cyclin box of yeast B-type and mammalian A- and B-type cyclins. In situ hybridization showed that cycMs3 mRNA can be detected only in proliferating cells and not in differentiated alfalfa cells. When differentiated G0-arrested cells were induced to reenter the cell cycle in the G1 phase and resume cell division by treatment with plant hormones, cycMs3 transcript levels increased long before the onset of DNA synthesis. In contrast, histone H3-1 mRNA and ...
"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): ...
Cell Cycle. 8 (24): 4155-67. doi:10.4161/cc.8.24.10316. PMC 2896895. PMID 19946220. Yao V, Berkman CE, Choi JK, O'Keefe DS, ... prostate cancer cell population harbors self-renewing long-term tumor-propagating cells that resist castration". Cell Stem Cell ... LNCaP cells express AR, but PC-3 and DU-145 cells express very little or no AR. The proliferation of LNCaP cells is androgen- ... Prostate cancer cells are generally devoid of zinc. Prostate cancer cells save energy by not making citrate, and use the ...
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. ( ...
Cell Cycle. 5 (1): 23-6. doi:10.4161/cc.5.1.2305. PMID 16357527. Kazanskaya O, Glinka A, del Barco Barrantes I, Stannek P, ... Cell. 7 (4): 525-34. doi:10.1016/j.devcel.2004.07.019. PMID 15469841. Jin YR, Turcotte TJ, Crocker AL, Han XH, Yoon JK (2011 ...
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 ...
"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. Chun-Zhi Z, ...
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 ...
"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. ( ...
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 ... 2002). "Clinical and cell line specific expression profiles of a human gene identified in experimental central nervous system ...
... 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 ...
Cell Cycle. 8 (22): 3742-9. doi:10.4161/cc.8.22.10047. PMID 19855176. Human CEP55 genome location and CEP55 gene details page ... doi:10.1016/j.cell.2006.09.026. PMID 17081983. S2CID 7827573. Chen CH, Lu PJ, Chen YC, et al. (2007). "FLJ10540-elicited cell ... Associates with Centralspindlin to Control the Midbody Integrity and Cell Abscission during Cytokinesis". Mol. Biol. Cell. 17 ( ... CEP55 is a mitotic phosphoprotein that plays a key role in cytokinesis, the final stage of cell division. GRCh38: Ensembl ...
... miR-449b and miR-34c on inducing down-regulation of cell cycle-related proteins and cycle arrests in SKOV3-ipl cell, an ovarian ... Lizé M, Klimke A, Dobbelstein M (September 2011). "MicroRNA-449 in cell fate determination" (PDF). Cell Cycle. 10 (17): 2874-82 ... Feng M, Yu Q (January 2010). "miR-449 regulates CDK-Rb-E2F1 through an auto-regulatory feedback circuit". Cell Cycle. 9 (2): ... Cell Cycle. 10 (17): 2858-64. doi:10.4161/cc.10.17.17011. PMID 21857154. Buechner J, Tømte E, Haug BH, Henriksen JR, Løkke C, ...
RNF7 and SETD3 as PCNA-associated proteins in human cells". Cell Cycle. 14 (15): 2509-19. doi:10.1080/15384101.2015.1053667. ... 2015). "Expression of histone methyltransferases as novel biomarkers for renal cell tumor diagnosis and prognostication". ... "SETD3 acts as a prognostic marker in breast cancer patients and modulates the viability and invasion of breast cancer cells". ... interfering RNA resulted in an inhibition of cytoskeletal function and invasiveness of triple-negative breast cancer cells. ...
... has two phases to its life-cycle: sexual and asexual.[8] The asexual stage (anamorph) grows in affected ... perforating the middle lamella but damage to either the plasmalemma or cell walls was not observed.[29] The disease is often ... "under the rules for the naming of fungi with pleomorphic life-cycles", the correct name should be Hymenoscyphus fraxineus.[1] ...
Hamming codes are only suitable for more reliable single-level cell (SLC) NAND. Denser multi-level cell (MLC) NAND requires ... The iterative decoding algorithm works best when there are not short cycles in the factor graph that represents the decoder; ... "Error Correction Code in Single Level Cell NAND Flash memories" 16 February 2007 ...
M phase of mitotic cell cycle. · mitotic prophase. · mitotic anaphase. · mitotic cell cycle. · apoptotic process. · cellular ... Halaschek-Wiener J, Brooks-Wilson A. Progeria of stem cells: stem cell exhaustion in Hutchinson-Gilford progeria syndrome. J. ... J. Cell. Sci. October 2000, 113 (19): 3473-84. PMID 10984438.. *^ Dreuillet C, Tillit J, Kress M, Ernoult-Lange M. In vivo and ... Cell. December 2002, 13 (12): 4401-13. PMC 138642. PMID 12475961. doi:10.1091/mbc.E02-07-0450.. ...
Other catenin, cadherin or cell cycle regulators may also be useful in treating a variety of cancers. While recent studies in ... F9 embryonal carcinoma cells are similar to the P19 cells shown in Figure 1 and normally have cell-to-cell adhesion mediated by ... A tumor cell line with defective δ-catenin, low levels of E-cadherin and poor cell-to-cell adhesion could be restored to normal ... providing the cell with a means of stable cell adhesion. However, decreases in this adhesion ability of the cell has been ...
Cells are homogenised in a blender and filtered to remove debris. *The homogenised sample is placed in an ultracentrifuge and ... used density gradient centrifugation to determine which isotope or isotopes of nitrogen were present in the DNA after cycles of ... General method of fractionation: Cell sample is stored in a suspension which is: *Buffered - neutral pH, preventing damage to ... This method is commonly used to separate organelles and membranes found in cells. Organelles generally differ from each other ...
Sertoli cell proliferation. • توصيل الإشارة. • peptide hormone processing. • positive regulation of gene expression. • cell- ... on the mouse estrous cycle". Regul. Pept. 81 (1-3): 67-71. PMID 10395410. doi:10.1016/S0167-0115(99)00022-1. ... positive regulation of cell migration. • positive regulation of transcription from RNA polymerase II promoter. • حمل أنثوي. • ... 1989). "Expression of biologically active human follitropin in Chinese hamster ovary cells". J. Biol. Chem. 264 (9): 4769-75. ...
The] clave pattern has two opposing rhythm cells: the first cell consists of three strokes, or the rhythm cell, which is called ... 8 (son) clave is shown on top and a beat cycle is shown below it. Any or all of these structures may be the emphasis at a given ... The second cell has two strokes and is called the two-side of the weak part of the clave. . . The different accent types in the ... Clave is the basic period, composed of two rhythmically opposed cells, one antecedent and the other consequent.[d][e] Clave was ...
They are a class of cell cycle-specific cytotoxic drugs that work by inhibiting the ability of cancer cells to divide: Acting ... The newer semi-synthetic chemotherapeutic agent vinorelbine is used in the treatment of non-small-cell lung cancer[7][9] and is ... "Safety and efficacy of vinorelbine in the treatment of non-small cell lung cancer". Clinical Medicine Insights: Oncology. 5 ...
Their life cycle is thought to begin with a virion attaching to specific cell-surface receptors such as C-type lectins, DC-SIGN ... dendritic cells and other cells including liver cells, fibroblasts, and adrenal gland cells.[93] Viral replication triggers ... doi:10.1016/j.cell.2014.10.006. PMC 4243531. PMID 25417101.. *^ a b c d e f g h Kühl A, Pöhlmann S (September 2012). "How Ebola ... liver cells, and several types of immune cells such as macrophages, monocytes, and dendritic cells are the main targets of ...
Cell Press. doi:10.1016/j.isci.2020.101234. Retrieved July 7, 2020.. Cite journal requires ,journal=. (help). ... The life cycle of a Bullfrog. Children Press. ISBN 978-0-87191-233-6 ...
Because the cell acquiring a chloroplast already had mitochondria (and peroxisomes, and a cell membrane for secretion), the new ... The Toc34 protein can then take up another molecule of GTP and begin the cycle again.[38] ... and therefore topologically outside of the cell, because to reach the chloroplast from the cytosol, you have to cross the cell ... "The Plant Cell. 12 (1): 53-64. doi:10.1105/tpc.12.1.53. PMC 140214. PMID 10634907.. ...
The retinoids appear to influence the cell life cycle in the follicle lining. This helps prevent the accumulation of skin cells ... Retinoids are medications that reduce inflammation, normalize the follicle cell life cycle, and reduce sebum production.[45][84 ... and Th1 cells.[45] IL-1α stimulates increased skin cell activity and reproduction, which, in turn, fuels comedo development.[45 ... and accumulation of skin cells in the hair follicle.[1] In healthy skin, the skin cells that have died come up to the surface ...
... has a general regulatory effect on the cell cycle.. *It increases MHC II and adhesion molecules LFA-1 and LFA-3 ( ... cells in destroying these B cells. When an NK cell latched onto the cap, it had an 80% success rate at killing the cell. In ... The antibody binds to the cell surface protein CD20. CD20 is widely expressed on B cells, from early pre-B cells to later in ... It induces apoptosis of CD20+ cells.. The combined effect results in the elimination of B cells (including the cancerous ones) ...
Outer hair cells serve as acoustic amplifiers for stimulation of the inner hair cells. Outer hair cells respond primarily to ... As a result, the reflex mechanism is activated again, and the cycle continues on. This ultimately leads to fatigue. ... "J. Cell Biol. 164 (6): 887-97. doi:10.1083/jcb.200310055. PMC 2172292. PMID 15024034.. ... The stereocilia (hair cells) of the inner ear can become subjected to bending from loud noises. Because they are not ...
Life cycle[edit]. Barnacles have two distinct larval stages, the nauplius and the cyprid, before developing into a mature adult ... Such barnacles feed by extending thread-like rhizomes of living cells into their hosts' bodies from their points of attachment. ... degrading to the condition of nothing more than sperm-producing cells.[15] ...
In medicine, this era brought innovations such as open-heart surgery and later stem cell therapy along with new medications and ... beginning a cycle of mutual advancement. The advancements in technology in this era allowed a more steady supply of food, ...
A k-cycle is a cycle of length k; for instance a 2-cycle is a digon and a 3-cycle is a triangle. A cycle graph is a graph that ... with a one in the cell for row i and column j when vertices i and j are adjacent, and a zero otherwise.[4]. adjacent. The ... Important special cases of cycles include Hamiltonian cycles, induced cycles, peripheral cycles, and the shortest cycle, which ... closely related to the cube-connected cycles.. C[edit]. C. Cn is an n-vertex cycle graph; see cycle.. cactus. A cactus graph, ...
The formation of the ascospores occurs through the conjugation of the haploid cells preceding the formation of the ascus.[8] ... of respiro-fermentative metabolism that consists of simultaneously generating energy from both respiration via the TCA cycle ... the yeast cells appear globose, ellipsoidal or cylindrical, 2-6 x 3-11 μm in size.[6] In a glucose-yeast extract broth, K. ... Alternatively, ascosporogensis can arise directly from diploid cells.[8] Each ascus contains 1-4 ascospores.[8] The ploidy of K ...
Cell cycleEdit. The Caulobacter cell cycle regulatory system controls many modular subsystems that organize the progression of ... Cell cycle regulation includes feedback signals that pace progression of the cell cycle engine to match progress of events at ... An essential feature of the Caulobacter cell cycle is that the chromosome is replicated once and only once per cell cycle. This ... The central feature of the cell cycle regulation is a cyclical genetic circuit-a cell cycle engine-that is centered around the ...
Early Notch signaling maintains progenitor cycling. Photoreceptor precursors come about through inhibition of Notch signaling ... Further complexity arises from the various interconnections among bipolar cells, horizontal cells, and amacrine cells in the ... ON bipolar cells or inhibit (hyperpolarize) OFF bipolar cells. Thus, it is at the photoreceptor-bipolar cell synapse where ... which releases a neurotransmitter called glutamate to bipolar cells. Farther back is the cell body, which contains the cell's ...
Several cells may live together, forming filaments (or colonies). Andres 09:28, 11 Aug 2004 (UTC). *If someone knows more (or ... They are a significant component of the marine nitrogen cycle and an important primary producer in many areas of the ocean, but ... In a colony, a term quite loosely defined, the cells are stuck together due to the extracellular polysacharides, whereas in ... the nitrogen-fixing protein complex may be packaged into specialized cells called heterocysts." Aren't bacteria single-celled? ...
Multiple tornadoes produced by the same storm cell are referred to as a "tornado family".[21] Several tornadoes are sometimes ... Most tornadoes from supercells follow a recognizable life cycle. That begins when increasing rainfall drags with it an area of ... Tornadic storms do not contain more lightning than other storms and some tornadic cells never produce lightning at all. More ... If a new mesocyclone develops, the cycle may start again, producing one or more new tornadoes. Occasionally, the old (occluded ...
... cell-cycle processes). PAX8 is shown to be involved in tumor cell proliferation and differentiation, signal transduction, ... regulation of metanephric nephron tubule epithelial cell differentiation. • cell differentiation. • mesonephric tubule ... positive regulation of metanephric DCT cell differentiation. • negative regulation of mesenchymal cell apoptotic process ... pancreatic islet cells and lymphoid cells.[8] PAX8 and other transcription factors play a role in binding to DNA and regulating ...
The generative cell in the pollen grain divides into two haploid sperm cells by mitosis leading to the development of the ... One year reproductive cycle:The genera includes Abies, Picea, Cedrus, Pseudotsuga, Tsuga, Keteleeria (Pinaceae) and Cupressus, ... Then, the first tracheids of the transition zone are formed, where the radial size of cells and thickness of their cell walls ... At fertilization, one of the sperm cells unites its haploid nucleus with the haploid nucleus of an egg cell. The female cone ...
... the number of cell types or morphology all proposed as possible metrics.[2][3][4] ... "Transpositional shuffling and quality control in male germ cells to enhance evolution of complex organisms". Annals of the New ...
The spirochetes may also induce host cells to secrete quinolinic acid, which stimulates the NMDA receptor on nerve cells, which ... burgdorferi sensu lato was previously thought to be hindered in its ability to be maintained in an enzootic cycle in California ... However, PCR tests are susceptible to false positive results, e.g. by detection of debris of dead Borrelia cells or specimen ... 2010). "Chapter 6, Structure, Function and Biogenesis of the Borrelia Cell Envelope". Borrelia: Molecular Biology, Host ...
1 × 12-cell tower (single-wide, built between 2000 and 2001), 2 × 18-cell towers (double-wide, built in 2000), and 1 × 6-cell ... Indirect open-cycle mode:[e] Intake from canal leading to the Kankakee River,[d][f] discharge to cooling canal leading to ... Direct open-cycle mode:[c] Intake from canal leading to the Kankakee River,[d] discharge directly to the Illinois River. The ... Closed-cycle mode:[h] Intake from return cooling canal leading back from Dresden Cooling Lake,[i] discharge to cooling canal ...
It differs from cycle to cycle because the number of wolf genes inherited in the animal differs greatly and is recorded in a ... Cytogenetics and Cell Genetics. 34: 178-192. doi:10.1159/000131806. PMID 7151489.. ... The breeding cycles of dogs and coyotes are not synchronized and this makes interbreeding uncommon. If interbreeding had been ... Wolfdogs do not have one common description of their appearance because it varies from one breeding cycle to the next.[13] ...
This cycling of matter is known as the biogeochemical cycle. To maintain nutrients in soil it is therefore important that feces ... A combination of bile and bilirubin, which comes from dead red blood cells, gives feces the typical brown color.[1][2] ... and the body starts expelling bilirubin from dead red blood cells, its matter acquires the familiar brown color.[2] ... and the dead epithelial cells from the lining of the gut.[1] ...
Nicholas C. Price, Lewis Stevens (1999). Fundamentals of Enzymology: The Cell and Molecular Biology of Catalytic Proteins ( ... Bridges, C.D. and Alvarez, R.A. (1987). "The visual cycle operates via an isomerase acting on all-trans retinol in the pigment ... "RPE65 is the isomerohydrolase in the retinoid visual cycle". Proc. Natl. Acad. Sci. USA 102: 12413-12418. PMID 16116091. ... trans-retinyl palmitate by homogenates of human retinal epithelial cells". J. Biol. Chem. 262: 53-58. PMID 3793734. ...
A central event in the eukaryotic cell cycle is the decision to commence DNA replication (S phase). Strict controls normally ... A central event in the eukaryotic cell cycle is the decision to commence DNA replication (S phase). Strict controls normally ... rapid division cycles of diminishing cell size). We discuss essential features of the mechanism that are responsible for ... rapid division cycles of diminishing cell size). We discuss essential features of the mechanism that are responsible for ...
Quantification of the proliferative characteristics of normal and malignant cells has been of interest to oncolo- gists and ... cancer cell cell cycle cytokine development flow cytometry proliferation tissue tumor Vivo ... Initially, cell cycle analysis was pursued enthusiastically in the hope of gener- ating information useful for the development ... Human tumors of the same type have proved highly variable, and the cytokinetic tools available for cell cycle analysis have ...
... the ordered sequence of events that occur in a cell in preparation for cell division. The cell cycle is a four-stage process in ... which the cell increases in size, copies its DNA, prepares to divide, and divides. Learn more about the cell cycle and the ... Cell cycle, the ordered sequence of events that occur in a cell in preparation for cell division. The cell cycle is a four- ... the cell is forced to undergo programmed cell death, or apoptosis. However, the cell cycle and its checkpoint systems can be ...
Unicellular organisms have to coordinate nuclear division, cytokinesis (cell separation) and DNA synthesis so that the correct ... Hartwell LH (1992) Defects in cell cycle checkpoints may be responsible for the genomic instability of cancer cells. Cell 71: ... cycle. Multicellular organisms, such as humans, also have to maintain the correct order of events within the cell cycle, and ... 1994) A cell cycle regulator potentially involved in genesis of many tumour types. Science 264:436-440.PubMedCrossRefGoogle ...
Cell cycle. Stifled by inhibitions.. Peters G.. Comment on. *p15INK4B is a potential effector of TGF-beta-induced cell cycle ...
Get inspiration for Cell Cycle Powerpoint Template. Browse through our huge selection of community templates or smoothly ... Cell Cycle. Transcript: The Cell Cycle!! 1st stage Interphase- 1st stage of cell cycle/ first period before cell divishion. ... cell cycle Cell. Transcript: cells go through a thing called interphase in this phase the cell gets its DNA copied and ... anaphase in a cell telophase in a cell Cell in phases interphase in cells The cell divides creating a complete copy the thought ...
Due to their affiliation with DNA, histones are important for successful cell replication, which takes place via the cell cycle ... which takes place via the cell cycle.. Cell Cycle Timing. The cell cycle consists of four phases (G1, S, G2 and M), all of ... the post-translational changes occur throughout the cell cycle.. The most typical kind of cell cycle phosphorylation is on H3s ... Histones and the Cell Cycle. News-Medical. ( ...
... John Farley,1 Laurent Ozbun,2 Goli Samimi,3 and Michael J. Birrer2 ... 2Cell and Cancer Biology Department, Medicine Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892 ... 3Cancer Prevention Fellowship Program and Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute ...
G0 is a separate phase of interphase that cells can enter to pause the cell cycle. If a cell is not fully-grown or does not ... Previous section Components of the Cell Cycle Next section Duration of the Cell Cycle ... What are the two major phases of the cell cycle and during which does cell copying take place? During which does cleavage take ... The two major phases of the cell cycle are interphase and M phase. During one portion of interphase, the cells DNA is copied. ...
General concepts / Cell cycle specificity CELL CYCLE SPECIFICITY. Cell cycle was presented by Dr. Holy in Foundations. Cancer ... CELL CYCLE SPECIFIC DRUGS (CCS; esp. plant alkaloids and antimetabolites), and CELL CYCLE NON-SPECIFIC DRUGS (CCNS; esp. ... cells spend a different percentage of time in each portion of the cell cycle *the percentages indicated in the figure are ... it is common to follow treatment with a CCNS drug with a CCS drug, so that cancer cells are recruited into the cell cycle, ...
The American Cancer Societys Peer Review Committee for Cell Cycle Growth Control analyzes cell cycle and cell cycle control ... Peer Review Committee for Cell Cycle and Growth Control (CCG). Areas Reviewed. *Cell cycle and cell cycle control mechanisms in ... Oncogenes and suppressor genes as their expression or products affect cell cycle events ... Growth factors, inhibitors, radiation, effects of signal transduction on the cell cycle ...
Curr Opin Cell Biol. 2015 Apr;33:19-25. doi: 10.1016/ Epub 2014 Nov 12. Research Support, Non-U.S. Govt; ... cell signaling, cell cycle regulation, and cancer. We show in this review that cellular, animal and molecular studies provided ... Cell cycle regulation of mitochondrial function.. Lopez-Mejia IC1, Fajas L2. ... which is fine tuned by members of the cell cycle regulators families. Currently, proteins such as cyclins, CDKs, or E2Fs are ...
Purchase Genetic Expression in the Cell Cycle - 1st Edition. Print Book & E-Book. ISBN 9780125437202, 9780323148924 ... Acetate Content of H4 in the Cell Cycle. V. H4 Acetate Content Varies during the Cell Cycle. VI. Acetate Turnover on H4 in the ... Cell Cycle Phase Distribution. IX. Cell Locomotion. X. Cytoskeletal Components. XI. Cell Surface Fibronectin. XII. Conclusions ... Modulation of Structure and Function of the Plasma Membrane in the Cell Cycle of Neuroblastoma Cells. I. Introduction. II. Cell ...
In a somatic (body) cell, the cell cycle takes roughly 24 hours to completes, starting with G1. In G1, cells become enlarged, ... The Cell Cycle. Cell division (mitosis) occurs through the following phases, each of which is characterized by unique events. ... Research characterizes iPS87 cell line as cancer-inducing, stem cell-like cell line ... As the cell cycle enters the mitotic stage, Wee1 (a G2 checkpoint kinase), is degraded alongside Emi1 (an early mitotic ...
We make it easy to give your old cell a new home  cycle your cell. We will even give you a prepaid shipping label so you can ... Americans have heard the call to cycle your cell, and they are turning in their old phones in bigger numbers every day, said ... When you cycle your cell at, we all benefit through resource conservation, solid waste reduction, ... We offer both individuals and non-profit groups the opportunity to send us old cell phones in working condition, and we pay ...
D) When they stop dividing, they do so at random points in the cell cycle, and they are not subject to cell cycle controls. ... E) When they stop dividing, they do so at random points in the cell cycle; they are not subject to cell cycle controls; and ... B) As cells become more numerous, the cell surface proteins of one cell contact the adjoining cells and they stop dividing. ... The data were obtained from a study of the length of time spent in each phase of the cell cycle by cells of three eukaryotic ...
If most of the cells in animal or plant tissues do not go ,to cell-cycle, what the factors could be to induce senescence? , I ... Can anyone tell me that if the cells in a mature animal or plant tissue still keep cell-division and cell-death to keep ... message was truncated but as of note: senescent cells (Hayflick cells) are not necessarily apoptotic. Many post-mitotic cells ... apoptosis vs cell-cycle. LOCKSHIN, RICHARD A YPRLBIO at Mon Sep 26 14:30:49 EST 1994 *Previous message: ...
In an interdisciplinary study they explain why the current concept of the bacterial cell cycle has to be rewritten. The results ... Researchers at the Biozentrum of the University have demonstrated how bacteria coordinate cell division with the replication of ... Although it is natural to think that the cell cycle begins with the birth of the cell and ends with the next cell division, the ... the duplication of a cells genetic information on the one hand and cell division on the other. Although the cell cycle in ...
... 929243. The Hubble space telescope (HST) solar array consists of ... The thermal cycle test was interrupted after 2,577 cycles, and a "cold-roll" test was performed on one of the modules in order ... Citation: Alexander, D., Edge, T., Willowby, D., and Gerlach, L., "Hubble Space Telescope Solar Cell Module Thermal Cycle Test ... an accelerated thermal cycle test in vacuum was conducted at NASAs Marshall Space Flight Center (MSFC), using two 128-cell ...
Cell cycle checkpoint protein, Rad1 (IPR003011). Short name: Cell_cycle_checkpoint_Rad1 ... A conserved checkpoint pathway mediates DNA damage--induced apoptosis and cell cycle arrest in C. elegans.. Mol. Cell 5 435-43 ... Rad1 is a component of the 9-1-1 cell-cycle checkpoint response complex, which plays a role in checkpoint activation that ... In Caenorhabditis elegans, the cell cycle checkpoint protein RAD1 homologue mrt-2 has a role in genome stability by promoting ...
Do you really want to delete this prezi? Neither you, nor the coeditors you shared it with will be able to recover it again. DeleteCancel ...
Areas of interest include gene therapy, cell kinetics, pharmacokinetics, chemotherapy, oncology, developmental biology, wound ... Piotr Widlak, "The DNA Damage-Induced Cell Cycle Checkpoints," Journal of Theoretical Medicine, vol. 2, no. 4, pp. 237-243, ... The DNA Damage-Induced Cell Cycle Checkpoints. Piotr Widlak Department of Experimental and Clinical, Radiobiology, Center of ...
... of the periodically expressed subunits differs significantly between organisms and is often mirrored by changes in cell-cycle- ... Our comparative analysis of eukaryotic cell-cycle complexes reveals that the identity ... Jensen, L., de Lichtenberg, U., Jensen, T. et al. Just-in-time assembly of cell-cycle protein complexes. Nat Prec (2008). https ... Just-in-time assembly of cell-cycle protein complexes. *Lars Jensen. 1. , ...
Proteomic Analysis of the Cell Cycle of Procylic Form Trypanosoma brucei Thomas W. M. Crozier, Michele Tinti, Richard J. ...
Cell Cycle RT2 Profiler PCR Array The Human Cell Cycle RT² Profiler PCR Array profiles the expression of 84 genes key to cell ... Cell Cycle RT2 Profiler PCR Array The Mouse Cell Cycle RT² Profiler PCR Array profiles the expression of 84 genes key to cell ... Cell Cycle RT2 Profiler PCR Array The Rat Cell Cycle RT² Profiler PCR Array profiles the expression of 84 genes key to cell ... Cell cycle dysregulation commonly occurs during oncogenesis, and tumor cells often do not arrest the cell cycle when normally ...
... in the progeny swarmer cell until later in the cell cycle when the swarmer cell differentiates into a new stalked cell (2, 3). ... This cell-cycle pattern of CtrA≈P distribution, and thus cell-cycle progression, is caused by temporally regulated ... As wild-type cells bearing pctrA290 progressed through the cell cycle, samples were pulse labeled with [35S]methionine at the ... Both are cell-cycle regulated, with the activity of the P1 promoter peaking in early predivisional cells and the activity of ...
... which control the cell cycle, cell death, cell metabolism and oxidative stress. This pathway appears to be well conserved ... Cell cycle and death control: long live Forkheads Trends Biochem Sci. 2002 Jul;27(7):352-60. doi: 10.1016/s0968-0004(02)02113-8 ...
The mitotic and meiotic cell cycle share many regulators, but there are also important differences between the two processes. ... Regulation of the meiotic cell cycle in oocytes Curr Opin Cell Biol. 2000 Dec;12(6):666-75. doi: 10.1016/s0955-0674(00)00150-2 ... The mitotic and meiotic cell cycle share many regulators, but there are also important differences between the two processes. ... been made recently into the signalling mechanisms that induce G2-arrested oocytes to resume and complete the meiotic cell cycle ...
... authors show that the transcription factor REST regulates cardiomyocyte proliferation by binding and repressing the cell cycle ... Here we show that REST also regulates the cardiomyocyte cell cycle. REST binds and represses the cell cycle inhibitor gene p21 ... e Immunostaining for cell cycle markers indicating that p21 inactivation rescues the cell cycle defect resulting from Rest ... g Immunostaining for cell cycle markers indicating p21 inactivation rescues the cell cycle defect resulting from Rest deletion ...
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  • If DNA damage or abnormalities in spindle formation are detected at these checkpoints, the cell is forced to undergo programmed cell death, or apoptosis . (
  • Hartwell LH, Weinert TA (1989) Checkpoints: Controls which ensure the order of cell cycle events. (
  • Murray AW (1992) Creative blocks: Cell cycle checkpoints and feedback controls. (
  • Hartwell LH (1992) Defects in cell cycle checkpoints may be responsible for the genomic instability of cancer cells. (
  • Key genes that regulate cell cycle progression and checkpoints encode cullins, cyclins, and cyclin-dependent kinases and their inhibitors. (
  • How cells use checkpoints at the end of G1 phase, end of G2 phase, and partway through M phase (the spindle checkpoint) to regulate the cell cycle. (
  • Cell proliferation includes a series of events that is tightly regulated by several checkpoints and layers of control mechanisms. (
  • Surveillance mechanisms stop progression through the cell cycle at specific checkpoints (at the G1 → S, G2 → M and metaphase → anaphase transitions) if certain crucial requirements have not been met. (
  • These cycles require the careful coordination of cell-processes checkpoints that prevent cells from dividing when something - DNA duplication, for example - has gone wrong. (
  • 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. (
  • Cell cycle checkpoints are regulatory pathways that control the order and timing of cell cycle transitions and ensure that critical events such as DNA replication and chromosome segregation are completed with high fidelity. (
  • In addition, checkpoints respond to damage by arresting the cell cycle to provide time for repair and by inducing transcription of genes that facilitate repair. (
  • Aguda BD (1999) Instabilities in phosphorylation‐dephosphorylation cascades and cell cycle checkpoints. (
  • Failure in the cell-cycle checkpoints leads to genomic instability and subsequent development of cancers from the initial affected cell. (
  • Cell cycle regulation of mitochondrial function. (
  • Currently, proteins such as cyclins, CDKs, or E2Fs are being studied in the context of cell proliferation and survival, cell signaling, cell cycle regulation, and cancer. (
  • and describe the use of conditional lethal mutants to study the regulation of the cell cycle of eukaryotic cells. (
  • The cell cycle relies on ubiquitin and the SCF complex plays an integral role in the regulation of this process. (
  • S-Phase Kinase Associated Protein 2 (Skp2), an FBP involved in cell cycle regulation, is one of the most highly studied FBPs. (
  • 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. (
  • QIAGEN provides a broad range of assay technologies for cell cycle research that enables analysis of gene expression and regulation, epigenetic modification, genotyping, and signal transduction pathway activation. (
  • The Human Cell Cycle RT² Profiler PCR Array profiles the expression of 84 genes key to cell cycle regulation. (
  • The Human Cell Cycle EpiTect Methyl II Signature PCR Array profiles the promoter methylation status of a panel of 22 genes key to cell cycle regulation. (
  • The Human Cell Cycle EpiTect Chip qPCR Array profiles the histone modification status or "histone code" of 84 genes key to cell cycle regulation. (
  • By elucidating the REST-p21 genetic mechanism underlying the cell cycle regulation of proliferating cardiomyocytes during cardiac development and regeneration, our study provides an opportunity for developing cell-based therapeutics for heart disease. (
  • 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. (
  • Conclusions: Our results show that CGGBP1 expression is important for cell cycle progression through multiple parallel mechanisms including the regulation of CDKN1A and GAS1 levels. (
  • The focus is on understanding how such diverse developmental inputs can modulate cell cycle regulation and, reciprocally, how a common way of regulating cell cycle progression can participate in different developmental strategies. (
  • Regulation of the Embryonic Cell Proliferation by Drosophila Cyclin D and Cyclin E Complexes (C. Lehner, et al. (
  • Cell Cycle Regulation in Early Mouse Embryos (J. Kubiak & M. Ciemerych). (
  • Biologists may have to change the way they view cell cycle regulation. (
  • Glyphosate-based pesticides affect cell cycle regulation. (
  • Glyphosate-based pesticides adversely affect cell cycle regulation at concentrations 500 to 4000 times lower than used in agriculatural applications. (
  • Several glyphosate-based pesticides from different manufacturers were assayed in comparison with Roundup 3plus for their ability to interfere with the cell cycle regulation. (
  • At the G1 to S-phase transition various stimuli such as DNA damage or growth factor withdrawal can result in a stop in cell cycle progression through regulation of Cyclin D-Cdk4/6 or Cyclin E-Cdk2 complex activity and the Retinoblastoma protein Rb. (
  • Tools to study aspects of the cell cycle include mitotic inhibitors, CDK inhibitors, apoptosis inducers and inhibitors , DNA intercalators and crosslinkers , kinase inhibitors, and other bioactive small molecules for cell cycle regulation . (
  • Increasing evidence points to the role of membrane transport in the regulation of cell cycle, differentiation and other aspects of cell physiology that shape the multistep tumor progression, such as resistance to apoptosis and cell invasiveness. (
  • Gene regulation during cell-cycle progression is an intricately choreographed process, ensuring accurate DNA replication and division. (
  • Employing genome-wide ribosome profiling, we uncover widespread translational regulation of hundreds of mRNAs serving as an unexpected mechanism for gene regulation underlying cell-cycle progression. (
  • A striking example is the S phase translational regulation of RICTOR, which is associated with cell cycle-dependent activation of mammalian target of rapamycin complex 2 (mTORC2) signaling and accurate cell-cycle progression. (
  • Our findings illuminate the prevalence and dynamic nature of translational regulation underlying the mammalian cell cycle. (
  • The proper regulation of brain cell numbers is one of earliest critical steps in fetal brain development. (
  • Finally, transcription factors within the nucleus must initiate the transcription of genes involved in cell proliferation. (
  • However, the cell cycle and its checkpoint systems can be sabotaged by defective proteins or genes that cause malignant transformation of the cell, which can lead to cancer . (
  • The replication independent histone genes are transcribed at a relatively constant low rate, regardless of cell cycle stage. (
  • However, most of the vertebrate histone genes are replication dependent and are therefore more highly expressed during the cell cycle's S phase. (
  • Therefore, NPAT could be the link between cell cycle machinery and shared heightened transcription of histone genes during S phase. (
  • Other cell cycle regulatory genes include apoptosis regulators and DNA damage sensors. (
  • Direct phosphorylation by PKB results in cytoplasmic retention and inactivation, inhibiting the expression of FOXO-regulated genes, which control the cell cycle, cell death, cell metabolism and oxidative stress. (
  • Focusing on the cyclin-dependent kinase 2 (cdk-2) and cyclin E (cye-1), we show that inhibition of cell cycle genes leads to tolerance towards environmental stress and longevity. (
  • Furthermore, we discovered that SKN-1 (ortholog of mammalian Nrf proteins) activates protective gene expression and induces longevity when cell cycle genes are inactivated. (
  • In addition, our studies suggest further roles of cell cycle genes beyond cell cycle progression and support the recently described connection of SKN-1/Nrf to signals deriving from the germline. (
  • Here, we used quantitative real-time PCR, profiling the expression of 93 genes in single-cells from three different cell lines. (
  • We found that the total transcript level per cell and the expression of most individual genes correlated with progression through the cell cycle, but not with cell size. (
  • Detailed analysis of cell cycle predictive genes allowed us to define subpopulations with distinct gene expression profiles and to calculate a cell cycle index that illustrates the transition of cells between cell cycle phases. (
  • In conclusion, we provide useful experimental approaches and bioinformatics to identify informative and predictive genes at the single-cell level, which opens up new means to describe and understand cell proliferation and subpopulation dynamics. (
  • CGGBP1 depletion also increased the expression of cell cycle regulatory genes CDKN1A and GAS1, associated with reductions in histone H3 lysine 9 trimethylation in their promoters. (
  • We identified mutations in the pavarotti (pav) and tumbleweed (tum) genes needed for cytokinesis by a phenotype of large and multinucleate cells in the embryonic epidermis and nervous system. (
  • Hoyt MA, Totis L and Roberts BT (1991) S. cerevisiae genes required for cell cycle arrest in response to loss of microtubule function. (
  • Levels of mRNA indicate which genes are active and what the cell is doing. (
  • They expected something like a messy knot of string, which would correspond to many genes being turned on and off multiple times throughout the cycle. (
  • We believe the specific cell-to-cell signaling and dysfunction observed in fruit flies is applicable to mammals, which also possess genes Notch and Cut," said Deng. (
  • 1 Functional promoter SNPs in cell cycle checkpoint genes. (
  • D ow nloaded from 2 A substantial number of genes mutated in human cancers encode components of the cell cycle processes. (
  • Since the G1/S transition in the cell cycle is a finely regulated biological process we hypothesized that sequence variations in the promoter region of the related genes might indeed lead to abnormal expression, thus predisposing the individuals carrying these genetic variants to cancer. (
  • In this report we screened the promoter regions of 16 cell cycle checkpoint genes for DNA variants and assessed the functional impact of these promoter SNPs (pSNPs) by combining in silico analysis and in vitro functional assays. (
  • This disomic region contains imprinted genes, including the gene encoding the cell cycle inhibitor p57 Kip2 ( CDKN1C ), which is silenced as a consequence of the recombination event. (
  • Courchesne noted that several hundred different genes coordinate the cell cycle network in the fetal brain. (
  • Both genetic mutations and non-genetic factors can change how these genes work and cause abnormal cell numbers and cell types. (
  • According to retired biology professor John W. Kimball, before a cell can undertake division, it must duplicate its genetic material so that each cell from the resulting division receives a full set of genes. (
  • When the genes are successfully duplicated, the cell is ready to begin dividing. (
  • When egg and sperm cells fuse, the two halves form a full set of genes. (
  • This interest stems from (a) the fact that cancer is a disease of uncontrolled proliferation, (b) the finding that many of the commonly used anticancer agents are preferentially toxic to cells that are actively proliferating, and (c) the observa- tion that significant differences in proliferation characteristics exist between normal and malignant cells. (
  • Multicellular organisms, such as humans, also have to maintain the correct order of events within the cell cycle, and must, in addition, regulate the growth and division of different tissues so that uncontrolled proliferation does not lead to tumorigenesis (3, 4). (
  • This complex task of controlling the timing of cell proliferation in response to both external stimuli and internal status is not yet fully understood. (
  • Specific cellular functions, such as proliferation, survival, growth, or senescence, require a particular adaptive metabolic response, which is fine tuned by members of the cell cycle regulators families. (
  • and the role of cell membrane and related subcellular elements in the control of proliferation, differentiation, and cell cycle kinetics. (
  • Despite the importance of cardiomyocyte proliferation in cardiac development and regeneration, the mechanisms that promote cardiomyocyte cell cycle remain incompletely understood. (
  • Rest deletion de-represses p21 and inhibits the cardiomyocyte cell cycle and proliferation in embryonic or regenerating hearts. (
  • We further show that p21 knockout rescues cardiomyocyte cell cycle and proliferation defects resulting from Rest deletion. (
  • In this study, we reveal that suppression of the cell cycle inhibitor gene p21 by REST is critically required during cardiac development and regeneration to maintain cardiomyocyte proliferation. (
  • Pardee AB (1974) A restriction point for control of normal animal cell proliferation. (
  • Zetterberg A and Larsson O (1985) Kinetic analysis of regulatory events in G1 leading to proliferation or quiescence of Swiss 3T3 cells. (
  • But when Cut garbles those signals the result is uncontrolled cell proliferation, sometimes with dire genetic and health consequences. (
  • Over the course of a year, they tracked the cell-to-cell communication in Drosophila egg chambers that control cell proliferation. (
  • The researchers traced the journey of transmissions originating from Notch """" which carries information gleaned from other cells """" following the signals down the Notch pathway as Cut linked them to the control of cell proliferation in the egg chambers, which they observed at different stages. (
  • Cell Proliferation 32: 321-335. (
  • Ethanol extract of Antrodia camphorata inhibits proliferation of HCT-8 human colorectal cancer cells. (
  • Withaferin A directly inhibits the proliferation and metastatic activity of gastric cancer cells. (
  • In mitosis, aurora kinases control chromatid segregation, thereby making these serine/threonine kinases essential for cell proliferation. (
  • Indeed, the only nuclear G1/S molecules are the cell cycle inhibitors, pRb, p57, and variably, p21: none of the cyclins or cdks necessary to drive human β-cell proliferation are present in the nuclear compartment. (
  • This observation may provide an explanation for the refractoriness of human β-cells to proliferation. (
  • Thus, in addition to known obstacles to human β-cell proliferation, restriction of G1/S molecules to the cytoplasm of the human β-cell represents an unanticipated obstacle to therapeutic human β-cell expansion. (
  • Accordingly, a major goal of diabetes research is to develop means to induce human β-cell proliferation and expansion, targeting either endogenous human β-cells or β-cells grown ex vivo. (
  • Further, we are only beginning to understand the physiological signals or mechanisms that activate and then inactivate this perinatal β-cell proliferation. (
  • As one example, we have only recently learned that loss of the platelet-derived growth factor (PDGF) receptor-α in adult human β-cells, with the resultant loss of ability to activate mitogen-activated protein kinase and methylation (Ezh2) and downstream cell cycle (p16) machinery, may underlie the refractoriness of human β-cells to proliferation ( 16 ). (
  • With the goal of understanding how best to encourage human β-cells to replicate, we and others previously delineated the repertoire of G1/S regulatory proteins present in the adult human islet and have used this information to develop a working model of the "human islet G1/S proteome" ( 12 , 14 - 29 ), hoping that it might be useful in developing therapeutic approaches to manipulating human β-cell proliferation. (
  • The G1/S model has proven useful in predicting approaches to driving human β-cell proliferation in in vitro and in vivo systems. (
  • Draw and label (identify) a cell in interphase. (
  • cancerous cells divide at a higher rate, therefore, more cells in the stage of interphase would suggest a higher effectiveness of chemotherapy. (
  • Without moving the slide, count the number of cells in interphase and each stage of mitosis and record below. (
  • Discuss the differences between interphase and stages of cell division. (
  • The stages G1, S, and G2 make up interphase, which accounts for the span between cell divisions. (
  • The two major phases of the cell cycle are interphase and M phase. (
  • G0 is a separate phase of interphase that cells can enter to pause the cell cycle. (
  • During which phase of interphase does cell growth occur? (
  • Cell growth occurs constantly throughout interphase. (
  • During the Interphase the cell grows and it makes copy of DNA, and it prepares to divide. (
  • Interphase is often included in discussions of mitosis, but interphase is technically not part of mitosis, but rather encompasses stages G1, S, and G2 of the cell cycle. (
  • In dividing Drosophila neural progenitors the apical-basal orientation of the mitotic spindle, the basal cortical localization of the cell fate determinants Numb and/or Prospero as well as the coordination of these events are mediated by several proteins which include Bazooka (Baz), Inscuteable (Insc) and Partner of Inscuteable (Pins) which localize as an apical cortical complex starting at interphase. (
  • 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 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. (
  • Interphase is the stage of the cell cycle that usually lasts the longest. (
  • During interphase, the cell may not look like it is doing much, but many significant events are happening to prepare it for cell division. (
  • Three subphases make up interphase.The cell grows during the G1, or first gap, phase. (
  • Cells spend 90 to 95 percent of the time in interphase, where DNA is synthesized and the cell doubles in mass before mitosis begins. (
  • The longest part of the cell cycle is interphase. (
  • During interphase, the cell undergoes a growth phase in which it acquires energy to copy DNA. (
  • During interphase, the cell may not look like it is doing much, but many signific. (
  • Cells starting at a resting state or G0, will proceed to Interphase (G1, S, G2) followed by the M phase (mitosis and cytokinesis). (
  • Together, these three stages comprise the interphase phase of the cell cycle. (
  • The cell cycle is divided into different stages with those particular to cell division defined as the Mitotic phase. (
  • As the cell cycle enters the mitotic stage, Wee1 (a G 2 checkpoint kinase), is degraded alongside Emi1 (an early mitotic inhibitor) when bound to the SCF complex. (
  • Many post-mitotic cells undergo apoptosis. (
  • The mitotic and meiotic cell cycle share many regulators, but there are also important differences between the two processes. (
  • 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. (
  • Some fibers cross the cell to form the mitotic spindle. (
  • During the mitotic phase, the replicated chromosomes, organelles, and cytoplasm separate into two new daughter cells. (
  • Some cells enter the G0 phase semi-permanently and are considered post-mitotic, e.g., some liver, kidney, and stomach cells. (
  • The word "post-mitotic" is sometimes used to refer to both quiescent and senescent cells. (
  • After G2, the cell progresses into M phase, mitosis, during which chromosomes condense, and become separated by the mitotic spindle. (
  • Children with focal hyperinsulinism of infancy display a dramatic, non-neoplastic clonal expansion of β cells that have undergone mitotic recombination, resulting in paternal disomy of part of chromosome 11. (
  • A central event in the eukaryotic cell cycle is the decision to commence DNA replication (S phase). (
  • Due to their affiliation with DNA, histones are important for successful cell replication, which takes place via the cell cycle. (
  • Histones can be classified as replication dependent or replication independent, which is decided by their expression pattern during the cell cycle. (
  • D) Cell division allows for lower rates of error per chromosome replication. (
  • Researchers at the Biozentrum of the University have demonstrated how bacteria coordinate cell division with the replication of their genetic material. (
  • Their findings show that, in bacteria, the cell cycle starts and ends with the initiation of DNA replication, with the cell division event occurring between two DNA replication events. (
  • They observed the behavior of individual E. coli cells over long periods of time and systematically quantified multiple variables describing growth, cell division and DNA replication for thousands of cell cycles in several growth conditions. (
  • one determining when the next cell division should occur, and the other determining when the next initiation of DNA replication should occur," explains Thomas Julou, head of the study. (
  • Rad1 is a component of the 9-1-1 cell-cycle checkpoint response complex, which plays a role in checkpoint activation that permits DNA-repair pathways to prevent cell cycle progression in response to DNA damage and replication stress [ PMID: 9311982 , PMID: 21978893 ]. (
  • 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. (
  • The transcriptional regulator CtrA controls several key cell-cycle events in Caulobacter crescentus , including the initiation of DNA replication, DNA methylation, cell division, and flagellar biogenesis. (
  • We propose that the P1 promoter is activated after the initiation of DNA replication in the early predivisional cell. (
  • The progeny- stalked cell immediately initiates DNA replication, whereas DNA replication is repressed in the progeny swarmer cell until later in the cell cycle when the swarmer cell differentiates into a new stalked cell ( 2 , 3 ). (
  • Thus, the swarmer-to-stalked cell transition is coincident with the initiation of DNA replication. (
  • A critical function of the CtrA response regulator is to bind to and repress the origin of replication in the swarmer cell and thus control the time of initiation of DNA replication ( 4 ). (
  • Mammalian checkpoint pathways that block cell cycle progression as a consequence of blocked deoxyribonucleic acid ( DNA ) replication and DNA damage. (
  • When Cut accurately transcribed the Notch signals, the cells progressed appropriately from the conventional mitosis (replication and division) to the specialized endocycle, where cells cease division but still replicate their DNA. (
  • These events include the duplication of its DNA (DNA replication) and some of its organelles, and subsequently the partitioning of its cytoplasm and other components into two daughter cells in a process called cell division. (
  • 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. (
  • R. Crabb , M. C. Mackey and A. Rey , Propagating fronts, chaos and multistability in a cell replication model, Chaos , 6 (1996), 477-492. (
  • Aguda BD (2001) Kick‐starting the cell cycle: from growth‐factor stimulation to initiation of DNA replication. (
  • The G2 to M-phase transition of the cell cycle can be blocked if DNA is damaged, thus preventing mitosis with damaged chromosomes after replication. (
  • 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. (
  • 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. (
  • We hypothesized that targeting p57 Kip2 could stimulate adult human β cell replication. (
  • Indeed, when we suppressed CDKN1C expression in human islets obtained from deceased adult organ donors and transplanted them into hyperglycemic, immunodeficient mice, β cell replication increased more than 3-fold. (
  • These findings provide a molecular explanation for the massive β cell replication that occurs in children with focal hyperinsulinism. (
  • These data also provided evidence that β cells from older humans, in which baseline replication is negligible, can be coaxed to re-enter and complete the cell cycle while maintaining mature β cell properties. (
  • Expansion of pancreatic β-cells is a key goal of diabetes research, yet induction of adult human β-cell replication has proven frustratingly difficult. (
  • The proteins that play a role in stimulating cell division can be classified into four groups- growth factors , growth factor receptors , signal transducers, and nuclear regulatory proteins ( transcription factors ). (
  • Cells use special proteins and checkpoint signaling systems to ensure that the cell cycle progresses properly. (
  • Ubiquitin ligase also regulates ubiquitinylation by stimulating the degradation of cell cycle proteins via the 26S proteasome. (
  • In G 1 , cells become enlarged, mRNA and new proteins are synthesized, and these are then used during the subsequent synthesis of DNA. (
  • As malignant cells evolve, both genetic and epigenetic mechanisms commonly affect the expression of cell cycle regulatory proteins, causing overexpression of cyclins and loss of expression of cdk inhibitors. (
  • In this phase, the cell increases its supply of proteins, increases the number of organelles (such as mitochondria, ribosomes), and grows in size. (
  • The cyclin dependent kinases, or cdks, are the proteins that drive the cell cycle. (
  • Rb holds onto another protein, E2F, which is necessary to make the proteins which will allow the cell to enter S phase. (
  • The cdks are also important in mitosis (M). They phosphorylate many proteins that are necessary for cells to separate their chromosomes and divide. (
  • Cells control Cdt1 and Geminin levels post-translationally, using ubiquitination to target the unwanted proteins for proteasomal degradation. (
  • Abgent has over fifteen years of experience producing recombinant proteins in E. coli and mammalian cells (CHO and HEK293, etc), and we have added a powerful yeast expression platform to our menu of services. (
  • Even though the investigators genetically silenced the proteins or blocked them with a drug in normal as well as cancerous tissues, the animals remained healthy, they report in the Oct. 16 issue of the journal Cancer Cell . (
  • The experiments targeted two related proteins, cyclin D1 and cyclin D3, that control cells' growth cycle. (
  • Many types of cancer have abnormal amounts of the proteins, spurring the cells to grow too rapidly and form tumors. (
  • The new results shown that the cancers' addiction to these proteins is an Achilles' heel that can be safely targeted with an inhibitor drug that halts cancer growth or causes cancer cells to die. (
  • Cyclin proteins act as "checkpoint" guards to control cell's cycle of rest, growth and division. (
  • When the cyclin D proteins were turned off using this technique, the addicted cancer cells shut down while normal cells were unaffected. (
  • S phase is the time when all the cell's chromosomes are replicated so significant cell growth occurs here, but during both G1 and G2 cell growth occurs. (
  • B) Cell division would allow for the orderly and efficient segregation of multiple linear chromosomes. (
  • If there are 20 centromeres in a cell at anaphase, how many chromosomes are there in each daughter cell following cytokinesis? (
  • Then in late S phase, the newly synthesized CcrM DNA methyltransferase brings the replicated chromosomes from the hemimethylated to the fully methylated state before cell division ( 6 , 7 ). (
  • The chromosomes move to the center of cell. (
  • Chromosomes are split and the other chromatids move to opposite poles of the cell. (
  • Each cell contain one chromosomes it divide into four cells. (
  • The chromosomes begins to far/ opposite sides of the cell. (
  • Spindle fibers align the chromosomes along the middle of the cell nucleus. (
  • The paired chromosomes separate at the kinetochores and move to opposite sides of the cell. (
  • The duplicated chromosomes become aligned in the center of the cell, spindle fibers attach themselves to the centromere of the chromosomes. (
  • The stage of mitosis in which the duplicated sets of chromosomes separate and two indentical groups move to opposite poles of the cell. (
  • A type of cell division that results in two daughter cells each having the same number and kind of chromosomes as the parent nucleus, typical of ordinary tissue growth. (
  • As proliferating cells transition from G1 to M, the DNA content will double as the chromosomes are duplicated. (
  • All cells have a nucleus, which contains chromosomes holding the plant's genetic information. (
  • As division progresses, the chromosomes in the nucleus are pulled apart, and each cell receives a full set of genetic material. (
  • As division concludes, new nuclei form around the chromosomes, and cell walls develop, dividing the two cells. (
  • However, cells end up with only half of the normal number of chromosomes. (
  • The scheduled activity of the cdks, which allows orderly transition between cell cycle phases, is controlled by their association with cyclins and cdk inhibitors, by their state of phosphorylation, and by ubiquitin-mediated proteolysis. (
  • The crucial role of the cdks has prompted great interest in the development of specific kinase inhibitors that would be expected to block cell cycle progression and induce growth arrest. (
  • Unicellular organisms have to coordinate nuclear division, cytokinesis (cell separation) and DNA synthesis so that the correct order of events is maintained (1, 2). (
  • Which of the following are primarily responsible for cytokinesis in plant cells but not in animal cells? (
  • The spindle fibers disperse, and cytokinesis or the partitioning of the cell may also begin during this stage. (
  • In animal cells, cytokinesis results when a fiber ring composed of a protein called actin around the center of the cell contracts pinching the cell into two daughter cells, each with one nucleus. (
  • 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. (
  • At the end of mitosis two new cells form by cytokinesis. (
  • The Cignal E2F Reporter Assay Kit is designed to monitor the activity of E2F-regulated signaling pathways in cultured cells. (
  • Eukaryotic cells respond to DNA damage by activating signaling pathways that promote cell cycle arrest and DNA repair. (
  • We conclude that both, germline absence and inhibition through impairment of cell cycle machinery results in longevity through similar pathways. (
  • Checkpoint pathways have components shared among all eukaryotes, underscoring the conservation of cell cycle regulatory machinery. (
  • Akt functions to promote cell survival through two distinct pathways. (
  • Recent advances in our understanding of the cell cycle reveal how fidelity is normally achieved by the coordinated activity of cyclin-dependent kinases, checkpoint controls, and repair pathways and how this fidelity can be abrogated by specific genetic changes. (
  • DNA synthesis occuring in the S phase is essential to passing on genetic information to daughter cells, but loss of genetic control of synthesis and the appearance of mutations can occur when regulatory feedback pathways are deregulated. (
  • For example, mutations in a protein called p53 , which normally detects abnormalities in DNA at the G1 checkpoint, can enable cancer-causing mutations to bypass this checkpoint and allow the cell to escape apoptosis. (
  • In Caenorhabditis elegans, the cell cycle checkpoint protein RAD1 homologue mrt-2 has a role in genome stability by promoting DNA double strand break-induced cell cycle arrest and apoptosis, and is required for maintaining telomere length and germline immortality [ PMID: 10882129 , PMID: 10646593 , PMID: 16951081 ]. (
  • The novel DNA damage checkpoint protein ddc1p is phosphorylated periodically during the cell cycle and in response to DNA damage in budding yeast. (
  • A conserved checkpoint pathway mediates DNA damage--induced apoptosis and cell cycle arrest in C. elegans. (
  • Cells in which checkpoint control is disrupted are more sensitive to additional genotoxic or microtubular damage. (
  • Here, we review key aspects of cell cycle and checkpoint control, as well as exploitable abnormalities commonly found in cancer, in order to focus on promising targets of new agents presently in clinical trial or under development. (
  • Walworth NC (2000) Cell‐cycle checkpoint kinases: checking in on the cell cycle. (
  • Checkpoint loss results in genomic instability and has been implicated in the evolution of normal cells into cancer cells. (
  • The current understanding of the mechanism and kinetics of the G1 checkpoint called the restriction point (R‐point) in mammalian cells is discussed. (
  • Mitosis is the process of how eukaryotic cells divide and replicate. (
  • On the basis of the stimulatory and inhibitory messages a cell receives, it "decides" whether it should enter the cell cycle and divide. (
  • The cell divide also split all into two new cells. (
  • Only cells in the nervous system and the imaginal cells that generate the adult body divide during larval stages, with larval tissues growing by increasing ploidy rather than cell number. (
  • Cells multiply by going through a four-step cycle: expanding in size, copying their genetic information, preparing to divide, and then finally dividing into two cells. (
  • A DNA-binding protein, Cut interprets and transcribes the developmental signals sent through the "Notch" gene, which regulates a layer of epithelial cells as they replicate and divide. (
  • One sign was the fact that cells can divide, even when parts of the cyclin-dependent kinase complex are removed. (
  • Heinemann added, "But we also noticed that occasionally cells did not divide, and that these cells still showed metabolic oscillations. (
  • The current view is too narrow and cannot explain why cells still divide when part of the cyclin-dependent kinase complex is removed. (
  • Play media 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. (
  • Many cells do not enter G0 and continue to divide throughout an organism's life, e.g., epithelial cells. (
  • The cell cycle is a complex and carefully controlled series of events that allows cells to grow and divide when they should (for example, in a growing baby) and not when they shouldn't. (
  • Cells that escape from cell cycle control, and divide whenever they want to, can become cancer cells. (
  • These signals (sometimes called growth factors) will tell the cell to divide, or to keep hanging out in G1. (
  • Some cells, like nerve and muscle cells, never divide and spend their entire lives in G1. (
  • In order for the cell to divide into two cells, two copies of DNA are needed, one for each cell. (
  • Blood cells divide rapidly, whereas nerve cells stop dividing once they have matured. (
  • These new hair cells appear to be derived from a support cell precursor which is stimulated to divide by events associated with hair cell loss. (
  • Cells divide following a series of defined steps that involve changes in protein expression, cell morphology, and DNA synthesis. (
  • How Do Plant Cells Divide? (
  • This is a graphical abstract, published with the Molecular Cell paper. (
  • In addition, the cell cycle must be coordinated with nutrient availability and differentiation into the meiotic, or sexual, cycle. (
  • Timing Cell-Cycle Exit and Differentiation in Oligodendrocyte Development (M. Raff, et al. (
  • To continue cell cycle and enter S phase Stop cell cycle and enter G0 phase for undergoing differentiation. (
  • M. Adimy , F. Crauste and C. Marquet , Asymptotic behavior and stability switch for a mature-immature model of cell differentiation, Nonlinear Analysis: Real World , 11 (2010), 2913-2929. (
  • When a cell stops dividing, having gone through what is know as "terminal differentiation", it. (
  • Hence, we will consider experimental papers, essays and reviews concerning the function of membrane transporters in cell cycle, differentiation, apoptosis, adhesion/migration, the metastatic process, the transition from stem cell to cancer cell and angiogenesis. (
  • Differentiation refers to the process by which cells acquire the ability to carry out a certain function. (
  • In plants, differentiation turns cells into flower buds, roots and leaves. (
  • Larry D. Noodén, in his book "Plant Cell Death Processes," credits cellular death with allowing for differentiation and protection from pathogens that, otherwise, could harm plants. (
  • Cell cycle dysregulation commonly occurs during oncogenesis, and tumor cells often do not arrest the cell cycle when normally required. (
  • Most tumor cells have a very high metabolism. (
  • 2OHOA increases sphingomyelin (SM) levels in the membranes of tumor cells, which typically display decreased SM membrane content, and remodeled membranes, compared with normal cells. (
  • Cell-cycle dysregulation is a hallmark of tumor cells and human cancers. (
  • Caffeic acid and caffeic acid phenethyl ester induce apoptosis and cell cycle arrest of breast cancer cells MDA-MB-231. (
  • REST binds and represses the cell cycle inhibitor gene p21 and is required for mouse cardiac development and regeneration. (
  • For a stimulatory signal to reach the nucleus and "turn on" cell division, four main steps must occur. (
  • Third, this activation must stimulate a signal to be transmitted, or transduced, from the receptor at the cell surface to the nucleus within the cell. (
  • Measurements of the amount of DNA per nucleus were taken on a large number of cells from a growing fungus. (
  • In which stage of the cell cycle did the nucleus contain 6 picograms of DNA? (
  • A group of cells is assayed for DNA content immediately following mitosis and is found to have an average of 8 picograms of DNA per nucleus. (
  • Our Fucci cell cycle reporters let you label just the nucleus, or both the nucleus and cytoplasm, allowing visualization of cell shape. (
  • In prokaryotes which lack a cell nucleus, the cell cycle occurs via a process termed binary fission. (
  • In this chapter, I will attempt to describe these fundamental mechanisms that control the cell cycle, and to relate them to the etiology of cancer development. (
  • Genetic Expression in the Cell Cycle provides an understanding of the molecular mechanisms that govern the expression of genetic information during the cell cycle. (
  • Computational modelling was then applied to this data to uncover the control mechanisms of the cell cycle. (
  • New insights have been made recently into the signalling mechanisms that induce G2-arrested oocytes to resume and complete the meiotic cell cycle. (
  • Recently we had found CGGBP1 to be a cell cycle regulatory midbody protein required for normal cytokinetic abscission in normal human fibroblasts, which have all the cell cycle regulatory mechanisms intact. (
  • By combining RNA interference and genetic mutations, we found that the role of CGGBP1 in cell cycle involves multiple mechanisms, as single deficiencies of CDKN1A, GAS1 as well as TP53, INK4A or ARF failed to rescue the G0/G1 arrest caused by CGGBP1 depletion. (
  • Several mechanisms have been identified in mammalian cells for the induction of apoptosis. (
  • This pathway card outlines the mechanisms through which cyclins and cyclin-dependent kinases (Cdks) regulate cell cycle progression at the G1 to S-phase transition. (
  • 2OHOA induces cell cycle arrest and apoptosis in several cancer cell lines, including glioma, leukemia, breast and colon cancer lines. (
  • Harmaline induces cell cycle arrest and apoptosis in SGC-7901 cells. (
  • Tea polyphenols induce S phase arrest and apoptosis in gallbladder cancer cells. (
  • Dysregulation of this process can result in the progressive transformation of normal cells into cancer cells. (
  • In the last decade, it has been repeatedly demonstrated that dysregulation of the cell cycle can cause injured kidneys to progress to CKD. (
  • Dysregulation of the cell cycle has been shown to result in a number of diseases, most notably cancer and other proliferative diseases. (
  • Pramparo said the new findings provide in vivo evidence for the involvement of cell cycle processes in ASD brain maldevelopment and significantly illuminate the complexities involved in early dysregulation and disruption of the developing ASD brain. (
  • The arrest might, at least partially, be attributed to DNA damage since activation of the DNA-damage response pathway leads to cell cycle arrest. (
  • Thus, controlled manipulation of this pathway holds promise for the expansion of β cells in patients with type 2 diabetes. (
  • Others were modified to develop a type of T-cell acute lymphoblastic leukemia (T-ALL) that is driven by an abnormal pathway known as Notch1. (
  • Upregulation of histone gene expression is one of the hallmarks of entry into the cell cycle's S phase. (
  • This process is assumed to be under the control of the cell cycle, because of how closely linked to the S phase histone synthesis is. (
  • Entry into the S phase in animal cells is regulated to a large extent by the cyclin E-CDK2 kinase complex. (
  • During M phase, or mitosis, the cell divides. (
  • If a cell that is in G1 is not biologically ready to continue on to S phase either because it has not reached a sufficient size or does not have the appropriate cellular environment, what does it do? (
  • If a cell is not fully-grown or does not have the appropriate cellular environment, it can enter G0 where it can stay for as long as is necessary to achieve appropriate cellular conditions before proceeding on to S phase. (
  • Quiescent and aging cells which are unable to replicate are said to be in resting phase or G 0 where they might stay for an indefinite length of time. (
  • At which phase are centrioles beginning to move apart in animal cells? (
  • E) the S phase of the cell cycle. (
  • During S phase, the stalked cell elongates and differentiates a new swarmer pole by activating a flagellar transcriptional cascade ( 5 ). (
  • By applying the random forests algorithm, a supervised machine learning approach, we show how a multi-gene signature that classifies individual cells into their correct cell cycle phase and cell size can be generated. (
  • CGGBP1 depletion by RNA interference in tumor-derived cells caused an increase in the cell population at G0/G1 phase and reduced the number of cells in the S phase. (
  • Viruses have evolved strategies to modulate cell cycle progression including stimulation of S phase entry from G1 or G0 or cell cycle arrest at G2/M for example. (
  • 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. (
  • During this phase, the biosynthetic activities of the cell, which are considerably slowed down during M phase, resume at a high rate. (
  • In G1 phase, a cell has three options. (
  • We consider a generational and continuous-time two-phase model of the cell cycle. (
  • The next phase of the cycle is S phase, during which DNA is synthesized, or replicated. (
  • After the cell escapes from G1 into S phase, it is usually going to go through the whole cell cycle and make two cells. (
  • In a special type of G1 phase, sometimes called a G0 phase, cells such as nerve cells never leave the first gap phase. (
  • The G2, or second gap, phase sees more cell growth. (
  • What Is the Longest Phase of the Cell Cycle? (
  • The longest phase of the cell cycle is the Gap 1 phase, or G1 phase. (
  • During this phase, the cell gears up for cell division by amassing more organelles and getting larger. (
  • What Type of Cell Enters the G0 Phase? (
  • Cells of all types may enter the G0 phase of the cell cycle. (
  • Cell division is part of the cell cycle, and it is caused either by binary fission or as part of a multiple-phase cycle. (
  • Using these markers we found evidence for reversible changes in cell cycle status throughout the cochlea, while progression through S phase and mitosis was restricted to the region of the cochlea which sustained hair cell loss. (
  • as cells transition into S phase, Cdt1 levels fall and Geminin levels rise, remaining high until the cells are back in G1. (
  • These probes allow precise, visual evaluation of the cell cycle phase. (
  • Expression of these probes causes cell nuclei to turn red during G1 phase and cyan during S, G2, and M phases, allowing complete visual tracking of the cell cycle. (
  • The Tali® Cell Cycle Kit includes a ready-to-use reagent that, when used with the Tali® Image-Based Cytometer, provides a convenient and accurate determination of the percentage of cells in each phase of the cell cycle. (
  • Consequently, the degree of fluorescence is proportional to the amount of cellular DNA, which itself is indicative of cell cycle phase (as cells progress through the cell cycle, the amount of DNA ultimately doubles). (
  • PI will also label RNA, so the addition of RNase A is necessary for accurate determination of the percentage of cells in each phase of the cell cycle. (
  • The G1 to S-phase transition of the cell cycle is tightly controlled. (
  • DNA binding dyes such as Propidium Iodide (PI), 7-AAD (7-aminoactinomycin) or DAPI are used to measure the change in DNA content of cell as they transition through GO, G1, S, G2 and M phase. (
  • More precisely, severe AKI causes PTCs to arrest in the G1/S or G2/M phase of the cell cycle, leading to maladaptive repair and a fibrotic outcome. (
  • Mitosis and the production of two daughter cells occur in M phase. (
  • is a supervised approach for PrEdicting cell cycle phase in a COntinuum using single-cell RNA sequencing data. (
  • object to perform cell cycle phase prediction. (
  • During the first phase, a band of fibers crosses the cell, marking the location of the further division. (
  • Our comparative analysis of eukaryotic cell-cycle complexes reveals that the identity of the periodically expressed subunits differs significantly between organisms and is often mirrored by changes in cell-cycle-dependent phosphorylation of the protein products. (
  • All textbooks describe the cyclin-dependent kinase complex as the one and only/exclusive regulator of the eukaryotic cell cycle. (
  • Phosphorylated CtrA (CtrA≈P) is present in the swarmer cell, rapidly disappears at the swarmer-to-stalked cell transition, and accumulates again in the predivisional cell. (
  • This network contains many positive feedback loops that generate a bistable switch in E2F activity which is similar to a toggle switch and explains the transition from growth‐factor‐dependent to growth‐factor‐independent transition of cell cycle progression at the R‐point. (
  • The restriction point (R‐point) marks the transition from growth‐factor‐dependent to growth‐factor‐independent cell cycle progression. (
  • What are the two major phases of the cell cycle and during which does cell copying take place? (
  • CDKs regulate the cell's progression through the phases of the cell cycle by modulating the activity of key substrates. (
  • Our cell cycle reporter vectors deliver fluorescent, ubiquitination-based, cell-cycle indicators (Fucci) that allow you to identify cells in various phases of the cell cycle. (
  • This Demonstration shows the phases of the cell cycle, emphasizing in particular the phases of mitosis leading to cell division. (
  • Each living cell grows and divides, thus generating new offspring. (
  • The cell cycle is a process in which a cell grows and divides to create a copy of itself. (
  • Plant growth occurs when one cell divides into two, differentiating into stems, leaves, flowers and roots. (
  • Once the cell has accumulated enough genetic material to supply two cells, as well as chloroplasts and other cellular structures for both cells, it undergoes a process called mitosis, during which a single cell divides into two. (
  • Similar to mitosis, during meiosis, one cell divides into two. (
  • The most typical kind of cell cycle phosphorylation is on H3's serine. (
  • Thus, two transcriptional feedback loops coupled to cell cycle-regulated proteolysis and phosphorylation of the CtrA protein result in the pattern of CtrA activity required for the temporal and spatial control of multiple cell-cycle events. (
  • a) Positively coupled phosphorylation‐dephosphorylation cycles of Cdc25A and Cdk2. (
  • Cell division (mitosis) occurs through the following phases, each of which is characterized by unique events. (
  • Cell cycle arrest most frequently occurs at the G1/S or G2/M boundaries. (
  • Nearly all cell division mutants in Drosophila were recovered in late larval/pupal lethal screens, with less than 10 embryonic lethal mutants identified, because larval development occurs without a requirement for cell division. (
  • 5. The method of claim 4 , wherein the step of introducing additional water occurs after the mixture has emerged from the fuel cell. (
  • Because plant cells are bound with a rigid cell wall, they are not reabsorbed after death, which occurs in animal cells. (
  • The cell cycle of the bacterium Caulobacter crescentus is accompanied by morphological transitions that produce an asymmetric predivisional cell. (
  • Cell Cycle Transitions in Early Xenopus Development (J. Maller, et al. (
  • The study of cell cycle controls in a number of experimental systems has led to the discovery that much of the basic machinery underlying control of the cell cycle has been conserved in all eukaryotic organisms (5). (
  • Components of the cell cycle machinery are frequently altered in human cancer. (
  • The Cell Cycle Machinery an Asymmetric Cell Division of Neural Progenitors in the Drosophila Embryonic Central Nervous System (W. Chia, et al. (
  • The cell cycle machinery and asym. (
  • Using established principles of biochemical kinetics, we compare the properties of this model in detail with the observed behavior of various mutant strains of fission yeast: wee1(-) (size control at Start), cdc13Delta and rum1(OP) (endoreplication), and wee1(-) rum1Delta (rapid division cycles of diminishing cell size). (
  • All organisms must control their cell division. (
  • Nurse P (1975) Genetic control of cell size and cell division in yeast. (
  • Lee MG, Nurse P (1987) Complementation used to clone a human homologue of the fission yeast cell cycle control gene cdc2. (
  • Serrano M, Hannon GL, Beach D (1993) A new regulatory motif in cell- cycle control causing specific inhibition of cyclin D/CDK4. (
  • This approach enabled the scientists to reveal the control mechanism of the bacterial cell cycle, but this method will be generally applicable to studying other biological processes and organisms. (
  • Caulobacter goes to great lengths to control the time and place of the activity of this critical regulatory factor during the cell cycle. (
  • We report here that ctrA expression is under the control of two promoters: a promoter (P1) that is active only in the early predivisional cell and a stronger promoter (P2) that is active in the late predivisional cell. (
  • Flagellin synthesis was assayed as an internal control for cell-cycle progression. (
  • Hartwell LH, Culotti J, Pringle JR and Reid BJ (1974) Genetic control of the cell division cycle in yeast. (
  • The Temporal Control of Cell Cycle and Cell Fate in Caenorhabditis Elegans (V. Ambros). (
  • Control of Cell Fate in Plant Meristems (M. Hobe, et al. (
  • A leading role played by metabolism also makes sense from an evolutionary perspective: "You would expect the earliest cells or proto-cells to have a simple control system to regulate division, and metabolism would be the obvious candidate. (
  • We further identified unappreciated coordination in translational control of mRNAs within molecular complexes dedicated to cell-cycle progression, lipid metabolism, and genome integrity. (
  • Crown antibodies pass additional stringent quality requirements, including extended control sets, uniform results against multiple biologically relevant cell lines and tissues, and function in multiple applications. (
  • Further underscoring the prenatal origins of Autism Spectrum Disorder (ASD), researchers at University of California, San Diego School of Medicine describe for the first time how abnormal gene activity in cell cycle networks that are known to control brain cell production may underlie abnormal early brain growth in the disorder. (
  • In the control toddlers, researchers found that variation in brain size significantly correlated with cell cycle and protein folding gene networks, potentially impacting neuron number and synapse development. (
  • In part, this reflects a lack of understanding of cell cycle control in the human β-cell. (
  • Here, we provide a comprehensive immunocytochemical "atlas" of G1/S control molecules in the human β-cell. (
  • More importantly, and in contrast to anticipated results, the human β-cell G1/S atlas reveals that almost all of the critical G1/S cell cycle control molecules are located in the cytoplasm of the quiescent human β-cell. (
  • Cell grows to the point that the DNA cannot control the whole cell effectively? (
  • In contrast to classical molecular biology approaches where the effects of mutations are analyzed, the current study uses a new approach in which analysis of the subtle fluctuations that normally growing cells exhibit is used to infer how the underlying process is controlled. (
  • Current Opinion in Cell Biology 12: 697-704. (
  • Trends in Cell Biology 10: 154-158. (
  • Trends in Cell Biology 10: 296-303. (
  • The cell cycle is one of the most studied processes in biology," says Professor Nikolaus Rajewsky, Scientific Director of MDC's Berlin Institute for Medical Systems Biology (BIMSB), who spearheaded the project. (
  • The findings come thanks to Rajewsky and molecular biologists in his Systems Biology of Gene Regulatory Elements Lab at BIMSB in the city center, teaming up with a physicist and a mathematician in the Mathematical Cell Physiology Lab at Buch campus. (
  • Cell Cycle is a biweekly peer-reviewed scientific journal covering all aspects of cell biology. (
  • Current Opinion in Cell Biology 13: 738-747. (
  • Try the links in the MadSci Library for more information on Cell Biology . (
  • During mitosis nuclear chromosomal separation and departmentalization of cytoplasm occur, and finally two distinct daughter cells are formed. (
  • Although most Fucci probes label only cell nuclei, we offer a truncated version of hGeminin that is able to migrate to the cytoplasm between S and M phases, enabling the morphology of the cell to be visualized. (
  • Cytoplasm duplicates, cell grows? (
  • There are two highly significant events that take place during the cell cycle, copying of cellular components and cleaving of the cell into two independent cells. (
  • For example, damage to DNA or the spindle apparatus normally triggers cell cycle arrest or apoptosis, depending on the degree of damage and the cellular context. (
  • Cell cycle , the ordered sequence of events that occur in a cell in preparation for cell division . (
  • For a newly evolving protist, what would be the advantage of using eukaryote-like cell division rather than binary fission? (
  • C) Cell division would be faster than binary fission. (
  • cell-division and let the cells become senescent? (
  • Strictly speaking, it describes a periodic repetition of two coordinated cycles: the duplication of a cell's genetic information on the one hand and cell division on the other. (
  • Although it is natural to think that the cell cycle begins with the birth of the cell and ends with the next cell division, the new research argues for a major shift in this concept. (
  • On cell division, one pole yields a swarmer cell, and the other pole yields a nonmotile stalked cell (Fig. 1 B ), each with different cell fates ( 1 ). (
  • Division of the asymmetric predivisional cell is preceded by the synthesis and assembly of the polar flagellum and the tubulin-like cell division protein, FtsZ ( 8 ). (
  • Precise activation and inactivation of CDKs at specific points in the cell cycle are required for orderly cell division. (
  • To identify cell-cycle components whose maternal pools are depleted in embryogenesis or that have specific functions in embryogenesis, we screened for mutants defective in cell division during embryogenesis. (
  • The cell is engaged in metabolic activity and performing its prepare for mitosis (the next four phases that lead up to and include nuclear division). (
  • It is when the loose DNA starts to gather to form chromatid, the DNA copies itself, the spindle fibers start to form, and the cell prepares itself for cell division. (
  • Spindle Positioning During the Symmetric First Cell Division of Caenorhabditis Elegans Embryos (P. Gonczy, et al. (
  • But now University of Groningen scientists have found evidence that a metabolic oscillator acts as the "conductor" of cell division. (
  • Cells go through repetitive cycles of DNA duplication, growth, and cell division. (
  • Heinemann reasoned that metabolic oscillations might set the pace for cell division. (
  • We argue that metabolism and the cyclin-dependent kinase complex are coupled oscillators, which together orchestrate the growth and division of eukaryotic cells. (
  • Both oscillations have their own natural frequency, and, under normal circumstances, these two oscillations are coupled and compromise with each other at a common frequency, which then governs the cell division process. (
  • The cell-division cycle is a vital process by which a single-celled fertilized egg develops into a mature organism, as well as the process by which hair, skin, blood cells, and some internal organs are renewed. (
  • What Causes Cell Division? (
  • A worldwide used product Roundup 3plus, based on glyphosate as the active herbicide, was suggested to be of human health concern since it induced cell cycle dysfunction as judged from analysis of the first cell division of sea urchin embryos, a recognized model for cell cycle studies. (
  • Multiple genetic changes occur during the evolution of normal cells into cancer cells. (
  • During the plant life cycle, genetic material and many of these structures must be duplicated and divided between two cells. (
  • As genetic material duplicates, the cell also checks it for errors. (
  • Cell cycle progression is regulated by the cyclic rise and fall of kinase expression, and their interaction with, and action on, their cyclin targets. (
  • Central players are the cyclin-dependent kinases (cdks), which govern the initiation, progression, and completion of cell cycle events. (
  • These permitted us to investigate the requirements for Cyclin E function in neuroblast cell fate determination, a role previously shown for a null Cyclin E allele. (
  • The cyclin-dependent kinase complex was identified as the regulator of these cell cycles, and in 2001 the Nobel Prize for Physiology or Medicine was awarded for this discovery. (
  • The overall picture Heinemann and his colleagues have sketched in the Molecular Cell article is a system, in which the metabolic oscillator pulls the cyclin-dependent kinase complex through its cycle and dynamically gate the occurrence of the different cell cycle events. (
  • You can think of the cyclin as the gas for the cell cycle car. (
  • Blocking cyclin D1 in the mice drove the breast cancer cells into a kind of permanent retirement called senescence, an irreversible halt to their growth cycle. (
  • Inhibiting cyclin D3 in the T-ALL leukemia mice caused the cancer cells to self-destruct -- a programmed death process called apoptosis. (
  • In addition to these tests with mouse cancers, the scientists found that the cyclin-D-inhibiting drug had similar effects on human blood cancer cells in the laboratory. (
  • Also unknown was whether normal cells could get along without cyclin D1: If not, treating cancer by targeting the protein might be too dangerous. (
  • The authors say the results show that blocking cyclin D "represents a highly selective anticancer strategy that specifically targets cancer cells without significantly affecting normal tissues. (
  • Quantification of the proliferative characteristics of normal and malignant cells has been of interest to oncolo- gists and cancer biologists for almost three decades. (
  • Unbridled cell cycle progression in the presence of such damage is usually lethal, which may explain the selective sensitivity of some cancer cells to DNA-damaging treatments. (
  • Results: In this study we explored the role of CGGBP1 in the cell cycle in various cancer cell lines. (
  • Marinopyrrole A induced apoptosis in Mcl-1-dependent cancer cells and sensitized cancer cells to ABT-737. (
  • The compound has no effect on SM levels in non-cancer cells. (
  • CPI-613 is an E1α pyruvate dehydrogenase (PDH) modulator that prevents cancer cells from metabolizing glucose for energy. (
  • DelSal G, Loda M and Pagano M (1996) Cell cycle and cancer: critical events at the G1 restriction point. (
  • This evolution is facilitated in cancer cells by loss of fidelity in the processes that replicate, repair, and segregate the genome. (
  • How cancer can be linked to overactive positive cell cycle regulators (oncogenes) or inactive negative regulators (tumor suppressors). (
  • Baicalein induces cancer cell apoptosis and cause cell cycle arrest. (
  • Combined use of lower concentrations of jerantinine A and γ-tocotrienol induced potent cytotoxic effects on U87MG cancer cells. (
  • Wasabi compounds may possess activity against the growth and cancer stem cells phenotypes of human pancreatic cancer cells. (
  • Xanthones from Garcinia mangostana fruit hulls were cytotoxic against cancer cell lines. (
  • In many types of cancer, an excess of cyclins allows cells to grow too fast and form tumors. (
  • Heinemann studied budding yeast cells cultivated in microfluidic channels. (
  • First, a growth factor must bind to its receptor on the cell membrane . (
  • The cell cycle kit is a ready to use reagent to monitor cell cycle consist of a detergent, Propidium Iodide (PI), and RNAse A. The detergent permeabilizes the cell membrane, allowing the PI to access the DNA. (
  • Nuclear membrane forms, spindle fibers retract, daughter cells begin to invaginate? (
  • Plant cells contain a cell wall, a rigid membrane that provides shape for the cell and controls the movement of substances in and out of the cell. (
  • Aguda BD and Tang Y (1999) The kinetic origins of the restriction point in the mammalian cell cycle. (
  • The translational landscape of the mammalian cell cycle. (
  • In this study, we identified cell cycle factors as potent regulators of health and longevity in C. elegans. (
  • In addition, only a handful of cell cycle regulators (e.g., p53, p21) have been thoroughly studied during renal repair. (
  • Steroid hormone signaling and the FOXO transcription factor DAF-16 were required for longevity associated with cell cycle inhibition. (
  • But if Notch-to-Cut communication and Cut transcription were dysfunctional, so, too, was the cell cycle. (
  • As wild-type cells bearing p ctrA 290 progressed through the cell cycle, samples were pulse labeled with [ 35 S]methionine at the indicated times, and β-galactosidase and flagellin synthesis was assessed by immunoprecipitation. (
  • Our study reveals a REST-p21 regulatory axis as a mechanism for cell cycle progression in cardiomyocytes, which might be exploited therapeutically to enhance cardiac regeneration. (
  • Because heart diseases are the number one cause of death worldwide 11 , it is important to identify the regulatory factors of the cardiomyocyte cell cycle, which may be used as therapeutic targets for these devastating conditions. (
  • Several of these processes change during the cell cycle, but unlike transcriptional changes, the post-translational changes occur throughout the cell cycle. (
  • Explore the processes of photosynthesis and respiration that occur within plant and animal cells. (
  • Although the cell cycle in plant and animal cells has been elucidated quite precisely in the past decades, it has remained unclear how these two processes are coordinated in bacteria. (
  • The process of cells multiplying is one of the most well-understood processes in life. (
  • Cells are capable of performing multiple processes at the same time. (
  • However, in reality, other biological processes are causing additional movement, that are uncoupled from the cell cycle, in a third dimension. (
  • Rare gene mutations capable of increasing or decreasing cell number and brain size have been reported for tiny percentages of all ASD individuals, but for the vast majority of ASD children, the genomic defects behind abnormal brain overgrowth or undergrowth have remained unknown. (
  • The new study points to a common underlying defective functional genomic network - cell cycle - in living ASD toddlers, which plays a central role in fetal brain development. (
  • The spindle fibers are like strings that stretch the cell. (
  • Spindle fibers that are attached to the centromeres shorten and separate the sister chromatids, spindle fibers that are not connected to a chromosome elongate to stretch the cell? (
  • For the first time, a study shows that this depiction is justified, as cells do display a circular pattern of gene expression while going through the cell cycle. (
  • However, the translational landscape of gene expression underlying cell-cycle progression remains largely unknown. (
  • for example, by allowing identi- fication of rapidly proliferating tumors against which cell cycle-specific agents could be used with maximum effec- tiveness and by allowing rational scheduling of cell cyc- specific therapeutic agents to maximize the therapeutic ratio. (
  • Unfortunately, several difficulties have prevented realiza- tion of the early promise of cell cycle analysis: Proliferative patterns of the normal and malignant tissues have been found to be substantially more complex than originally an- ticipated, and synchronization of human tumors has proved remarkably difficult. (
  • Human tumors of the same type have proved highly variable, and the cytokinetic tools available for cell cycle analysis have been labor intensive, as well as somewhat subjective and in many cases inapplicable to humans. (
  • The cell cycle can be divided into four stages: G1, S, G2 and mitosis, while cells resting are termed quiescent cells (G0). (
  • 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). (
  • Here we show that REST also regulates the cardiomyocyte cell cycle. (
  • Analysis of cell cycle, via monitoring the quantity of DNA is routinely performed by flow cytometry and is a common assay for the platform. (
  • Hence, an understanding of the molecular interactions involved may suggest ways to sensitize cells to the effects of these compounds. (
  • Their results were published online in the journal Molecular Cell on December 15. (
  • Molecular Cell , online December 15, 2016. (
  • However, this failure of cell cycle arrest responses in malignant cells can also be exploited therapeutically. (
  • All of these cell-cycle events are controlled by a single protein, the essential response regulator CtrA ( 9 - 11 ). (
  • however, the involvement of the cell cycle regulator in asymmetric cell divisions has not been previously shown. (
  • Here we present evidence from ongoing experiments which suggest a requirement for the key cell cycle regulator cdc2 in asymmetric cell divisions. (
  • The plasmid-based vector, pTRE-CellCycle, allows tightly controlled, tetracycline (Tet)-inducible expression of two Fucci probes from a bidirectional promoter that can be induced using any Tet-On or Tet-Off technology. (
  • The newly replicated cells retained properties of mature β cells, including the expression of β cell markers such as insulin, PDX1, and NKX6.1. (
  • E) Binary fission would not allow the organism to have complex cells. (
  • Their promoter activity during the cell cycle is governed by a subtype-specific consensus element (SSCE). (
  • The ensuing accumulation of CtrA results in the activation of the P2 promoter and the repression of the P1 promoter late in the cell cycle. (
  • By observing stained cells, these stages can be observed in a eukaryotic plant cell. (
  • Thus, most mutants perturbing mitosis or the cell cycle do not manifest a phenotype until the adult body differentiates in late larval and pupal stages. (