Cell Cycle: 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.Cell Cycle Proteins: 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.Cell Cycle Checkpoints: 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.G1 Phase: 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.S Phase: 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.Mitosis: 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.Cyclins: 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.Cell Division: The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.Menstrual Cycle: 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.G2 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.Cyclin-Dependent Kinase Inhibitor p21: 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.Apoptosis: 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.Cyclin-Dependent Kinase Inhibitor p27: 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.Retinoblastoma Protein: 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.Cell Proliferation: All of the processes involved in increasing CELL NUMBER including CELL DIVISION.G2 Phase Cell Cycle Checkpoints: 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.G0 Phase: A quiescent state of cells during G1 PHASE.CDC2 Protein Kinase: 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.Cell Line, Tumor: A cell line derived from cultured tumor cells.G1 Phase Cell Cycle Checkpoints: 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.Tumor Suppressor Protein p53: 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.Cyclin-Dependent Kinase 2: 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.Protein-Serine-Threonine Kinases: A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.Cyclin D1: 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.Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.DNA Replication: The process by which a DNA molecule is duplicated.Cyclin E: A 50-kDa protein that complexes with CYCLIN-DEPENDENT KINASE 2 in the late G1 phase of the cell cycle.Genes, cdc: 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).DNA Damage: 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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Cyclin A: 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.Interphase: 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).DNA-Binding Proteins: 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.Cyclin B: 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.Molecular Sequence Data: 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.Flow Cytometry: 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: 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.Nuclear Proteins: 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.Tumor Suppressor Proteins: 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.Signal Transduction: 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.CDC2-CDC28 Kinases: 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.Estrous Cycle: 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).cdc25 Phosphatases: A subclass of dual specificity phosphatases that play a role in the progression of the CELL CYCLE. They dephosphorylate and activate CYCLIN-DEPENDENT KINASES.Cell Nucleus: 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)Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Mutation: 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, Cultured: 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.Tumor Cells, Cultured: 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.E2F Transcription Factors: 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.HeLa Cells: 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.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Cyclin B1: A cyclin B subtype that colocalizes with MICROTUBULES during INTERPHASE and is transported into the CELL NUCLEUS at the end of the G2 PHASE.Saccharomyces cerevisiae: 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, Messenger: 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.Models, Biological: 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.Gene Expression Regulation: 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.Transcription, Genetic: The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.Cyclin D: 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.DNA: 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).Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.Citric Acid Cycle: 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.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Cell Survival: 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.Bromodeoxyuridine: 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.E2F1 Transcription Factor: 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.Amino Acid Sequence: 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.Saccharomyces cerevisiae Proteins: 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.Blotting, Western: 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.S Phase Cell Cycle Checkpoints: 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.Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein.Down-Regulation: 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.Protein Binding: 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.Cyclin D3: A broadly expressed type D cyclin. Experiments using KNOCKOUT MICE suggest a role for cyclin D3 in LYMPHOCYTE development.Cyclin-Dependent Kinase Inhibitor Proteins: 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.Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.Antineoplastic Agents: Substances that inhibit or prevent the proliferation of NEOPLASMS.Fungal Proteins: Proteins found in any species of fungus.Transfection: 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.Schizosaccharomyces: A genus of ascomycetous fungi of the family Schizosaccharomycetaceae, order Schizosaccharomycetales.Histones: 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.M Phase Cell Cycle Checkpoints: The cellular signaling system that halts the progression of cells through MITOSIS or MEIOSIS if a defect that will affect CHROMOSOME SEGREGATION is detected.Proliferating Cell Nuclear Antigen: 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.Gene Expression Regulation, Neoplastic: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.Microtubule-Associated Proteins: 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.Proto-Oncogene Proteins: 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.Gene Expression Profiling: The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.Hydroxyurea: An antineoplastic agent that inhibits DNA synthesis through the inhibition of ribonucleoside diphosphate reductase.RNA, Small Interfering: 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.Cyclin-Dependent Kinase Inhibitor p16: 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.Caulobacter crescentus: A species of gram-negative, aerobic bacteria that consist of slender vibroid cells.Cyclin-Dependent Kinase 6: 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.Promoter Regions, Genetic: 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.Cyclin D2: 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.Transcription Factor DP1: 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.Mimosine: 3-Hydroxy-4-oxo-1(4H)-pyridinealanine. An antineoplastic alanine-substituted pyridine derivative isolated from Leucena glauca.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Ubiquitin-Protein Ligase Complexes: 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).Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.RNA Interference: 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.Kinetics: The rate dynamics in chemical or physical systems.Retinoblastoma-Binding Protein 1: 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.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Spindle Apparatus: 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.DNA Repair: 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.Life Cycle Stages: 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.Anaphase-Promoting Complex-Cyclosome: 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.Reverse Transcriptase Polymerase Chain Reaction: 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 Fusion Proteins: 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.Oligonucleotide Array Sequence Analysis: 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.Schizosaccharomyces pombe Proteins: 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.Centrosome: 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).Proto-Oncogene Proteins c-myc: 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: Nocodazole is an antineoplastic agent which exerts its effect by depolymerizing microtubules.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.3T3 Cells: 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.Cyclin A2: A widely-expressed cyclin A subtype that functions during the G1/S and G2/M transitions of the CELL CYCLE.Microscopy, Fluorescence: 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.CDC28 Protein Kinase, S cerevisiae: 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.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Repressor Proteins: 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.Gene Expression Regulation, Fungal: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in fungi.Ataxia Telangiectasia Mutated Proteins: 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.Checkpoint Kinase 2: 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.Enzyme Activation: 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.Gene Expression Regulation, Developmental: 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.Caulobacter: 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.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Genes, Fungal: The functional hereditary units of FUNGI.Chromatin: 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.S-Phase Kinase-Associated Proteins: 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.Up-Regulation: 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.Cell Aging: 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.Gamma Rays: 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.DNA Primers: 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.Proteins: 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.Sequence Homology, Amino Acid: The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.ThymidineNeoplasm Proteins: 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.Aphidicolin: 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 Transformation, Neoplastic: 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.Cyclin-Dependent Kinase Inhibitor p57: 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.Microtubules: 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.Cytoplasm: 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)Retinoblastoma-Like Protein p107: 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.Neoplasms: 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.Antineoplastic Agents, Phytogenic: Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.Breast Neoplasms: Tumors or cancer of the human BREAST.Retinoblastoma-Like Protein p130: A negative regulator of the CELL CYCLE that undergoes PHOSPHORYLATION by CYCLIN-DEPENDENT KINASES. RBL2 contains a conserved pocket region that binds E2F4 TRANSCRIPTION FACTOR and E2F5 TRANSCRIPTION FACTOR. RBL2 also interacts with viral ONCOPROTEINS such as POLYOMAVIRUS TUMOR ANTIGENS; ADENOVIRUS E1A PROTEINS; and PAPILLOMAVIRUS E7 PROTEINS.Proto-Oncogene Proteins c-bcl-2: 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.Meiosis: 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.Intracellular Signaling Peptides and Proteins: 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.Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.Cyclin G: A cyclin subtype that is found associated with CYCLIN-DEPENDENT KINASE 5; cyclin G associated kinase, and PROTEIN PHOSPHATASE 2.Immunoblotting: 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.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Growth Inhibitors: 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).Genes, p53: Tumor suppressor genes located on the short arm of human chromosome 17 and coding for the phosphoprotein p53.Ultraviolet Rays: 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.Cloning, Molecular: 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.HCT116 Cells: Human COLORECTAL CARCINOMA cell line.Trans-Activators: Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.Proteasome Endopeptidase Complex: 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.Tubulin: 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.Kinetin: A furanyl adenine found in PLANTS and FUNGI. It has plant growth regulation effects.Stem Cells: Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.Fluorescent Antibody Technique: 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.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Cell Line, Transformed: 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.Transcriptional Activation: Processes that stimulate the GENETIC TRANSCRIPTION of a gene or set of genes.Ubiquitin-Protein Ligases: 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.Gene Deletion: 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.Gene Knockdown Techniques: 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.Proto-Oncogene Proteins c-mdm2: 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.DNA, Fungal: Deoxyribonucleic acid that makes up the genetic material of fungi.E2F2 Transcription Factor: 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.Embryo, Nonmammalian: The developmental entity of a fertilized egg (ZYGOTE) in animal species other than MAMMALS. For chickens, use CHICK EMBRYO.Protein Structure, Tertiary: 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.Oocytes: 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).Mice, Knockout: 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.Embryo, Mammalian: 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.Cell Size: The quantity of volume or surface area of CELLS.Nucleic Acid Synthesis Inhibitors: Compounds that inhibit cell production of DNA or RNA.Drosophila Proteins: 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.Oncogene Proteins: Proteins coded by oncogenes. They include proteins resulting from the fusion of an oncogene and another gene (ONCOGENE PROTEINS, FUSION).Mitotic Index: An expression of the number of mitoses found in a stated number of cells.Chromosomal Proteins, Non-Histone: 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: 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.Gene Silencing: Interruption or suppression of the expression of a gene at transcriptional or translational levels.Ki-67 Antigen: 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.Cell Growth Processes: Processes required for CELL ENLARGEMENT and CELL PROLIFERATION.Metaphase: 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.PhosphoproteinsEpithelial Cells: 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.Mice, Nude: 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.Cyclin A1: A cyclin A subtype primarily found in male GERM CELLS. It may play a role in the passage of SPERMATOCYTES into meiosis I.Temperature: 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, Neoplasm: DNA present in neoplastic tissue.Mice, Inbred C57BLGene Products, vpr: 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.Cyclin G1: 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.HL-60 Cells: 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)

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 ...
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 ...
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 ...
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
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
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
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 ...
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 ...
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. ...
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 ...
TY - JOUR. T1 - The PI3K-Akt-mTOR pathway regulates a oligomer induced neuronal cell cycle events. AU - Bhaskar, Kiran. AU - Miller, Megan. AU - Chludzinski, Alexandra. AU - Herrup, Karl. AU - Zagorski, Michael. AU - Lamb, Bruce T.. PY - 2009/4/13. Y1 - 2009/4/13. N2 - Accumulating evidence suggests that neurons prone to degeneration in Alzheimers Disease (AD) exhibit evidence of re-entry into an aberrant mitotic cell cycle. Our laboratory recently demonstrated that, in a genomic amyloid precursor protein (APP) mouse model of AD (R1.40), neuronal cell cycle events (CCEs) occur in the absence of beta-amyloid (A) deposition and are still dependent upon the amyloidogenic processing of the amyloid precursor protein (APP). These data suggested that soluble A species might play a direct role in the induction of neuronal CCEs. Here, we show that exposure of non-transgenic primary cortical neurons to A oligomers, but not monomers or fibrils, results in the retraction of neuronal processes, and ...
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 ...
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 ...
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.
Pluripotency transcription programs by core transcription factors (CTFs) might be reset during M/G1 transition to maintain the pluripotency of embryonic stem cells (ESCs). However, little is known about how CTFs are governed during cell cycle progression. Here, we demonstrate that the regulation of Oct4 by Aurora kinase b (Aurkb)/protein phosphatase 1 (PP1) during the cell cycle is important for resetting Oct4 to pluripotency and cell cycle genes in determining the identity of ESCs. Aurkb phosphorylates Oct4(S229) during G2/M phase, leading to the dissociation of Oct4 from chromatin, whereas PP1 binds Oct4 and dephosphorylates Oct4(S229) during M/G1 transition, which resets Oct4-driven transcription for pluripotency and the cell cycle. Aurkb phosphor-mimetic and PP1 binding-deficient mutations in Oct4 alter the cell cycle, effect the loss of pluripotency in ESCs, and decrease the efficiency of somatic cell reprogramming. Our findings provide evidence that the cell cycle is linked directly to ...
Yeast Cdc7 protein kinase and Dbf4 protein are both required for the initiation of DNA replication at the G1/S phase boundary of the mitotic cell cycle. Cdc7 kinase function is stage-specific in the cell cycle, but total Cdc7 protein levels remained unchanged. Therefore, regulation of Cdc7 function appears to be the result of posttranslational modification. In this study, we have attempted to elucidate the mechanism responsible for achieving this specific execution point of Cdc7. Cdc7 kinase activity was shown to be maximal at the G1/S boundary by using either cultures synchronized with alpha factor or Cdc- mutants or with inhibitors of DNA synthesis or mitosis. Therefore, Cdc7 kinase is regulated by a posttranslational mechanism that ensures maximal Cdc7 activity at the G1/S boundary, which is consistent with Cdc7 function in the cell cycle. This cell cycle-dependent regulation could be the result of association with the Dbf4 protein. In this study, the Dbf4 protein was shown to be required for ...
1. Sherr CJ (1996) Cancer cell cycles. Science 274: 1672-1677. doi: 10.1126/science.274.5293.1672 8939849. 2. Sherr CJ, McCormick F (2002) The RB and p53 pathways in cancer. Cancer Cell 2: 103-112. doi: 10.1016/s1535-6108(02)00102-2 12204530. 3. Ren B, Cam H, Takahashi Y, Volkert T, Terragni J, et al. (2002) E2F integrates cell cycle progression with DNA repair, replication, and G(2)/M checkpoints. Genes Dev 16: 245-256. doi: 10.1101/gad.949802 11799067. 4. Dimova DK, Stevaux O, Frolov MV, Dyson NJ (2003) Cell cycle-dependent and cell cycle-independent control of transcription by the Drosophila E2F/RB pathway. Genes Dev 17: 2308-2320. doi: 10.1101/gad.1116703 12975318. 5. Korenjak M, Taylor-Harding B, Binne UK, Satterlee JS, Stevaux O, et al. (2004) Native E2F/RBF complexes contain Myb-interacting proteins and repress transcription of developmentally controlled E2F target genes. Cell 119: 181-193. doi: 10.1016/j.cell.2004.09.034 15479636. 6. van den Heuvel S, Dyson NJ (2008) Conserved functions ...
E2-2 alteration influences cell cycle exit of progenitors in vivo. (A)E2-2 overexpression increased cell cycle exit (EdU+Ki67-/EdU+) among the progenitor cell
BC: Thats what the cell cycle does!. FC: Cell Cycle. 1: What is the cell cycle? , The cell cycle is a process in which a cell grows and divides to create a copy of itself. Some orangisms reproduce through the cell cycle and in complex multicellular organisms, the cell cycle is used to allow the organism to grow and to reproduce worn out cells.. 2: Interphase , During interphase, a cell increase in mass, replicates its DNA, and prepares prophase.. 4: Prophase , 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.. 6: Metaphase , The duplicated chromosomes become aligned in the center of the cell, spindle fibers attach themselves to the centromere of the chromosomes.. 8: Anaphase , The stage of mitosis in which the duplicated sets of chromosomes separate and two indentical groups move to opposite poles of the cell.. 10: Telophase , A nuclear membrane re-forms around each new group of ...
BC: Thats what the cell cycle does!. FC: Cell Cycle. 1: What is the cell cycle? , The cell cycle is a process in which a cell grows and divides to create a copy of itself. Some orangisms reproduce through the cell cycle and in complex multicellular organisms, the cell cycle is used to allow the organism to grow and to reproduce worn out cells.. 2: Interphase , During interphase, a cell increase in mass, replicates its DNA, and prepares prophase.. 4: Prophase , 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.. 6: Metaphase , The duplicated chromosomes become aligned in the center of the cell, spindle fibers attach themselves to the centromere of the chromosomes.. 8: Anaphase , The stage of mitosis in which the duplicated sets of chromosomes separate and two indentical groups move to opposite poles of the cell.. 10: Telophase , A nuclear membrane re-forms around each new group of ...
The observability condition, which describes the cancer cell cycle kinetic state, is developed for determination of the initial cell age vectors. This cond
0.05, C< 0.01 vs. the control group). Analysis ... Cell cycle analysis The cells were cultured in a six-well plate for 24 hours and then incubated with different ratios of CIK (10:1, 20:1, or 30:1) for 72 hours. The cells were then digested, resuspended, incubated with P-gp antibodies for 30?moments at 4C, and washed twice in PBS. As demonstrated in Table?1, CIK cells caused a significant dose-dependent build up of A549 cells in the G2/M phases, lightly in the G0/G1, and a decrease of H phases from 1:10 to 1:30 at 48 hours Rilpivirine (Fig?3.) The variations in cell cycle distribution between the A549 and CIK treated A549 cells Rilpivirine were statistically significant (< 0.01). This indicated that CIK cells affected the distribution of A549 cells in each phase of the cell cycle, especially at higher concentrations (Table?1). Table 1 Effect of CIK cells on cell cycle distribution in A549 cells Number 3 The effect of cell cycle progress in A549 by cytokine-induced monster cells. Cell cycle ...
0.05, C< 0.01 vs. the control group). Analysis ... Cell cycle analysis The cells were cultured in a six-well plate for 24 hours and then incubated with different ratios of CIK (10:1, 20:1, or 30:1) for 72 hours. The cells were then digested, resuspended, incubated with P-gp antibodies for 30?moments at 4C, and washed twice in PBS. As demonstrated in Table?1, CIK cells caused a significant dose-dependent build up of A549 cells in the G2/M phases, lightly in the G0/G1, and a decrease of H phases from 1:10 to 1:30 at 48 hours Rilpivirine (Fig?3.) The variations in cell cycle distribution between the A549 and CIK treated A549 cells Rilpivirine were statistically significant (< 0.01). This indicated that CIK cells affected the distribution of A549 cells in each phase of the cell cycle, especially at higher concentrations (Table?1). Table 1 Effect of CIK cells on cell cycle distribution in A549 cells Number 3 The effect of cell cycle progress in A549 by cytokine-induced monster cells. Cell cycle ...
Takes two to Tango: the tale of ApiAP2 transcription factors and the regulation of crucial cell cycle functions in the apicomplexan parasite Toxoplasma ...
Biomedical engineers report a significant advance in efforts to repair a damaged heart after a heart attack, using grafted heart-muscle cells to create a repair patch. The key was overexpressing a gene that activates the cell-cycle of the grafted muscle cells, so they grow and divide more than control grafted cells. Up to now, an extremely low amount of engraftment of cardiomyocytes has been a stumbling block in hopes to use grafted cells to repair hearts after a heart attack. Without the successful repair that a graft could potentially offer, the damaged heart is prone to later heart failure and patient death. In experiments in a mouse model, researchers showed that gene overexpression of the cell-cycle activator CCND2 increased the proliferation of grafted cardiomyocytes. This led to increased remuscularization of the heart at the dead-tissue site of the heart attack, a larger graft size, improved cardiac function and decreased size of the dead tissue, or infarct. Besides regenerating muscle, ...
University of Iowa News. June 1, 2006. UI Cancer Researchers Receive Grant To Study Cell Cycle Checkpoints University of Iowa Roy J. and Lucille A. Carver College of Medicine researchers in the UI Holden Comprehensive Cancer Center have been awarded a five-year, $1.5 million grant from the National Cancer Institute to investigate a new hypothesis about how the mammalian cell cycle is regulated.. The cell cycle is the normal, orderly growth and division of cells. This process, also known as proliferation, is usually tightly controlled, but in cancers the process goes awry and malignant cells proliferate in an uncontrolled manner. Understanding the genetic and biochemical mechanisms that govern the cell cycle could lead to new and better cancer therapies that kill cancer cells but are not toxic to normal cells. The research team, led by Prabhat Goswami, Ph.D., UI assistant professor of radiation oncology in the Free Radical and Radiation Biology Graduate Program, will test the idea that reactive ...
Circadian oscillation and cell cycle progression are the two most essential rhythmic events present in almost all organisms. Circadian rhythms keep track of time and provide temporal regulation with a period of about 24 h. The cell cycle is optimiz
Click to view full text. Objective: The fermented wheat germ extract, which is the active ingredient of nutraceuticals widely used by cancer patients in Europe, Korea and the United States, possesses cytotoxic and anti-metastatic effects in various human malignancies. In estrogen responsive MCF-7 breast cancer cells, it has been shown to potentiate the induction of apoptosis by tamoxifen. However, its effects in triple-negative and Her2-overexpressing breast cancer cells and interactions with chemotherapy have not been investigated until now.. Methods: Cytotoxicity of Avemar lyophilisate alone and in combination with docetaxel was assessed by MTT and clonogenic assays in MCF-7 estrogen responsive, HCC-38 triple-negative and SKBR-3 Her2/neu overexpressing cells. Cell cycle phase distribution was determined by FACS. Apoptosisassociated activaton of caspase-3/7 was measured by Caspase-Glo Assay. Inhibition of tumor cell invasion was quantified using the ORIS Cell Invasion kit.. Results: Avemar ...
Although cells posterior to the SMW are normally quiescent, cell cycle re-entry occurs after tissue damage (Fan and Bergmann, 2008). Expression of the pro-apoptotic gene hid with the GMR promoter, which is expressed posterior to the MF (supplementary material Fig. S1A), induces extensive cell death (Fig. 1E,F). Dying, caspase-positive cells with pyknotic nuclei are extruded from the basal surface of the eye disc (supplementary material Fig. S1B,C), as in other discs (Gibson and Perrimon, 2005; Shen and Dahmann, 2005). Not all cells posterior to the SMW die, and some overcome cell cycle inhibition and re-enter S phase in a wave of proliferation (Fig. 1D,D′; Fan and Bergmann, 2008). GMR-hid flies are nearly eyeless (Fig. 1C), indicating that increased proliferation cannot fully compensate for tissue loss, probably because GMR-hid expression during pupal stages induces extensive apoptosis after the potential to re-enter the cell cycle is lost. Thus, GMR-hid eye discs behave somewhat differently ...
TY - JOUR. T1 - PARP1 promoter links cell cycle progression with adaptation to oxidative environment. AU - Pietrzak, Julita. AU - Spickett, Corinne M.. AU - Płoszaj, Tomasz. AU - Virág, László. AU - Robaszkiewicz, Agnieszka. PY - 2018/9. Y1 - 2018/9. N2 - Although electrophiles are considered as detrimental to cells, accumulating recent evidence indicates that proliferating non-cancerous and particularly cancerous cells utilize these agents for pro-survival and cell cycle promoting signaling. Hence, the redox shift to mild oxidant release must be balanced by multiple defense mechanisms. Our latest findings demonstrate that cell cycle progression, which dictates oxidant level in stress-free conditions, determines PARP1 transcription. Growth modulating factors regulate CDK4/6-RBs-E2Fs axis. In cells arrested in G1 and G0, RB1-E2F1 and RBL2-E2F4 dimers recruit chromatin remodelers such as HDAC1, SWI/SNF and PRC2 to condense chromatin and turn off transcription. Release of retinoblastoma-based ...
Our current understanding of the origin and evolution of the cell cycle is largely filled with gaps and unresolved questions. Numerous similarities between the processes comprising the cell cycle in distant organisms from the Pro- and Eukaryota kingdoms provide some clues about the course that evolution has taken. Contemporary Prokaryotes and Eukaryotes regulate their cell cycles in a quite similar way, using a master oscillator that regulates cell division. Despite this striking similarity, they use entirely different molecules for this purpose. The necessity to keep the master oscillator intact for the survival of every cell/organism allows evolutionary changes in only the secondary mechanisms and processes of the cell cycle. This is especially clear in oocytes and embryos, which have a direct impact on the reproductive success of an adult organism. Here, we present examples of cues driving such mild evolutionary changes of certain aspects of cell cycle progression in oocytes and early embryos. We
TC Hsieh, J Kunichki, Z Darzynkiewicz, JM Wu.. Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY, USA.. OBJECTIVE: The goal of this in vitro study was to test the cytostatic and cytotoxic activities of extracts derived from the polysaccharopeptide (PSP), Im-Yunity (Integrated Chinese Medicine Holdings Ltd., Kowloon, Hong Kong) prepared from strain Cov-1 of the mushroom Coriolus versicolor. DESIGN: Different volumes of 70% ethanol and water extracts of Im-Yunity were incubated with cultures of human promyelocytic leukemic HL-60 cells, and compared to nontreated control cells. At various times after treatment, cells were harvested and analyzed with respect to: (1). proliferation and cell cycle phase distribution, (2). induction of apoptosis, and (3). changes in expression of the immunomodulating cytokines interleukin (IL)-1 beta, IL-6, and IL-8. To test whether extracts also affected normal cells, similar experiments were also performed using isolated ...
The second group of cell cycle regulatory molecules are negative regulators. Negative regulators halt the cell cycle. Remember that in positive regulation, active molecules cause the cycle to progress.. The best understood negative regulatory molecules are retinoblastoma protein (Rb), p53, and p21. Retinoblastoma proteins are a group of tumor-suppressor proteins common in many cells. The 53 and 21 designations refer to the functional molecular masses of the proteins (p) in kilodaltons. Much of what is known about cell cycle regulation comes from research conducted with cells that have lost regulatory control. All three of these regulatory proteins were discovered to be damaged or non-functional in cells that had begun to replicate uncontrollably (became cancerous). In each case, the main cause of the unchecked progress through the cell cycle was a faulty copy of the regulatory protein.. Rb, p53, and p21 act primarily at the G1 checkpoint. p53 is a multi-functional protein that has a major impact ...
Self renewing mESCs are characterized by the coordinated expression of core pluripotency transcription factors and the establishment of a specific cell cycle program that allows rapid cell proliferation [1-3, 13, 14]. Here we present a novel pathway that links Oct4 and miR-335 with the Retinoblastoma pathway in self-renewing and differentiating mESCs.. In self-renewing mESC, cell cycle regulation is mainly executed by Cdk2 that mediates the hyperphosphorylation and biochemical inactivation of Retinoblastoma family protein [12-14]. The induction of cell differentiation is paralleled by a massive downregulation of total Oct4 and pRb levels and the acquisition of a Retinoblastoma pathway-regulated cell cycle program [11-14]. We show that RNAi-mediated knockdown of pRb from self-renewing mESCs reduces self-renewal potential, recapitulating effects normally observed upon Oct4 depletion or the induction of mESC differentiation. This indicates that high pRb protein levels improve the self-renewal ...
Temporo-spatial cell-cycle kinetics in HeLa cells irradiated by Ir-192 high dose-rate remote afterloading system (HDR-RALS)Temporo-spatial cell-cycle kinetics in HeLa cells irradiated by Ir-192 high dose-rate remote afterloading system (HDR-RALS) ...
Cell proliferation demands that the cells go through the mitotic cell cycle, involving duplication of their DNA before chromosome segregation and cell division. During G1 phase the decision is made whether to start a new round of the cell cycle, go into a quiescent state or enter into meiosis. It is critical for the cells to carefully regulate the progression through G1 phase, where the cells become committed to a new round in the cell cycle. Cell cycle progression is negatively regulated by checkpoint mechanisms to make sure that the events of one cell cycle phase have been completed before continuing to the next phase. Checkpoints delay the cell cycle in response to several forms of stress. DNA damage checkpoints are thought to allow additional time for DNA repair before DNA replication (S phase) and before chromosome segregation (mitosis). These responses are crucial for the cells to maintain their genetic integrity. The fact that the majority of cancer cells have defects in G1-S checkpoints ...
View Notes - Cell Cycle from BIOL 101 at UNC. Cell Cycle, Mitosis Meiosis Tuesday, February 10, 2009 10:19 AM 1. Cell Cycle aka Life of a Cell o Interphase Secreting Not dividing o Mitosis Nuclear
BioAssay record AID 461873 submitted by ChEMBL: Cell cycle arrest in human HeLa cells assessed as increase in S phase accumulation at 10 uM after 24 hrs by FACS analysis.
The eukaryotic cell cycle requires precise temporal coordination of the activities of hundreds of executor proteins (EPs) involved in cell growth and division. Cyclin-dependent protein kinases (Cdks) play central roles in regulating the production, activation, inactivation and destruction of these EPs. From genome-scale data sets of budding yeast, we identify 126 EPs that are regulated by Cdk1 both through direct phosphorylation of the EP and through phosphorylation of the transcription factors that control expression of the EP, so that each of these EPs is regulated by a feed-forward loop (FFL) from Cdk1. By mathematical modelling, we show that such FFLs can activate EPs at different phases of the cell cycle depending of the effective signs (+ or -) of the regulatory steps of the FFL. We provide several case studies of EPs that are controlled by FFLs exactly as our models predict. The signal-transduction properties of FFLs allow one (or a few) Cdk signal(s) to drive a host of cell cycle responses in
The second group of cell cycle regulatory molecules are negative regulators. Negative regulators halt the cell cycle. Remember that in positive regulation, active molecules cause the cycle to progress.. The best understood negative regulatory molecules are retinoblastoma protein (Rb), p53, and p21. Retinoblastoma proteins are a group of tumor-suppressor proteins common in many cells. The 53 and 21 designations refer to the functional molecular masses of the proteins (p) in kilodaltons. Much of what is known about cell cycle regulation comes from research conducted with cells that have lost regulatory control. All three of these regulatory proteins were discovered to be damaged or non-functional in cells that had begun to replicate uncontrollably (became cancerous). In each case, the main cause of the unchecked progress through the cell cycle was a faulty copy of the regulatory protein.. Rb, p53, and p21 act primarily at the G1 checkpoint. p53 is a multi-functional protein that has a major impact ...
Accumulating evidence suggests that neurons prone to degeneration in Alzheimers Disease (AD) exhibit evidence of re-entry into an aberrant mitotic cell cycle. Our laboratory recently demonstrated that, in a genomic amyloid precursor protein (APP) mouse model of AD (R1.40), neuronal cell cycle events (CCEs) occur in the absence of beta-amyloid (Aβ) deposition and are still dependent upon the amyloidogenic processing of the amyloid precursor protein (APP). These data suggested that soluble Aβ species might play a direct role in the induction of neuronal CCEs. Here, we show that exposure of non-transgenic primary cortical neurons to Aβ oligomers, but not monomers or fibrils, results in the retraction of neuronal processes, and induction of CCEs in a concentration dependent manner. Retraction of neuronal processes correlated with the induction of CCEs and the Aβ monomer or Aβ fibrils showed only minimal effects. In addition, we provide evidence that induction of neuronal CCEs are autonomous to primary
PINK1 and Parkin are established mediators of mitophagy, the selective removal of damaged mitochondria by autophagy. PINK1 and Parkin have been proposed to act as tumor suppressors, as loss-of-function mutations are correlated with enhanced tumorigenesis. However, it is unclear how PINK1 and Parkin act in coordination during mitophagy to influence the cell cycle. Here we show that PINK1 and Parkin genetically interact with proteins involved in cell cycle regulation, and loss of PINK1 and Parkin accelerates cell growth. PINK1- and Parkin-mediated activation of TBK1 at the mitochondria during mitophagy leads to a block in mitosis due to the sequestration of TBK1 from its physiological role at centrosomes during mitosis. Our study supports a diverse role for the far-reaching, regulatory effects of mitochondrial quality control in cellular homeostasis and demonstrates that the PINK1/Parkin pathway genetically interacts with the cell cycle, providing a framework for understanding the molecular basis ...
Regulatory molecules governing early cell cycle progression, such as cyclin D1/Cdk4/pRb, are frequent targets of genetic alterations in cancer (21). As such, the cell cycle regulatory pathway may represent a useful target for drug and gene therapy approaches. The flavone P276-00 has been evaluated here for antitumor activity in vitro and in vivo. In vitro evaluation was done in 16 tumor cell lines using PI assay and in 22 human tumor xenograft-derived panel using a clonogenic assay. Its antiproliferative activity was compared with cisplatin, a standard chemotherapeutic drug used in almost all advanced cancers. Cisplatin exerts its antitumor effects via the formation of DNA adducts and cross-links. Cisplatin-induced DNA damage results in cell cycle arrest, primarily at the S and G2 checkpoints, providing the opportunity for DNA damage repair before mitosis (22, 23). Unrepairable DNA damage often results in activation of the apoptotic pathway. In 16 human tumor cell lines and 22 human tumor ...
Cell cycle models used in biology can be very complex. These models have parameters with initially unknown values. The values of the parameters vastly aect the accuracy of the models in representing real biological cells. Typically people search for the best parameters to these models using computers only as tools to run simulations. In this thesis methods and results are described for a computer program that searches for parameters to a series of related models using well tested algorithms. The code for this program uses ODRPACK for parameter estimation and LSODAR to solve the dierential equations that comprise the model ...
ST7 has been proposed as a tumor suppressor gene at the chromosome region 7q31.1-q31.2. In order to gain some insight into its role in cancer, localization and verification of ST7 expression levels were performed. Various types of ST7 expression vectors tagged with sequences of GFP, YFP or V5 were created using gateway cloning system and full length ST7 cDNA isolated from a human adult brain cDNA library. Cytosolic ST7 expression in HCT-116, MCF-7 and PC-3 cell lines was detected via the fluorescence signal of the fusion proteins. ST7 translocation from cytoplasm to nucleus has not been observed in any of the conditions assayed. A cell cycle synchronization study demonstrated that both ST7 and SERPINE1 were over expressed when cells were arrested. Expression of these genes was found to be substantially diminished when the cells re-entered cell division status. In addition, we also found that Survivin, MMP13, and CyclinD1 were differentially expressed during cell cycle. Our findings suggest that ...
Chromosomes undergo dramatic morphological changes as cells advance through the cell cycle. Using powerful molecular and computational methods, several recent studies revealed an outstanding complexity of continuous structural changes accompanying cell cycle progression. In agreement with cell division being a fundamental cellular process, characteristic features of cell cycle stage‐specific genome structure are conserved from yeast to mouse. These studies further shine light on the critical roles that SMC complexes, already well known as fundamental regulators of chromosome topology, have in orchestrating structural dynamics throughout the cell cycle.. See also: L Lazar-Stefanita et al (September 2017) Y Kakui et al (2017),. SA Schalbetter et al (September 2017),. T Nagano et al (July 2017) ...
The protein encoded by this gene belongs to the Ser/Thr protein kinase family. It is required for checkpoint mediated cell cycle arrest in response to DNA damage or the presence of unreplicated DNA. This protein acts to integrate signals from ATM and ATR, two cell cycle proteins involved in DNA damage responses, that also associate with chromatin in meiotic prophase I. Phosphorylation of CDC25A protein phosphatase by this protein is required for cells to delay cell cycle progression in response to double-strand DNA breaks. Several alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Oct 2011 ...
Cellular systems biology aims to uncover design principles that describe the properties of biological networks through interaction of their components in space and time. The cell cycle is a complex system regulated by molecules that are integrated into functional modules to ensure genome integrity and faithful cell division. In budding yeast, cyclin-dependent kinases (Cdk1/Clb) drive cell cycle progression, being activated and inactivated in a precise temporal sequence. In this module, which we refer to as the Clb module, different Cdk1/Clb complexes are regulated to generate waves of Clb activity, a functional property of cell cycle control. The inhibitor Sic1 plays a critical role in the Clb module by binding to and blocking Cdk1/Clb activity, ultimately setting the timing of DNA replication and mitosis. Fifteen years of research subsequent to the identification of Sic1 have lead to the development of an integrative approach that addresses its role in regulating the Clb module. Sic1 is an ...
Time‐lapse imaging of cell‐cycle phase transitions reveals that phase durations are uncoupled and can be modeled as an Erlang process. Phase coupling can be forced by perturbing a strong cell‐cycle regulator acting on multiple phases.. See full publication here.. ...
We examined the molecular basis underlying cAMP and cGMP regulation of SMC proliferation and clearly showed that the main effect of cGMP is suppression of cyclin D1 and cdk4 activity, which leads to a delay in cdk2 activation and G1/S transition in the cell cycle. In contrast, cAMP inhibits both cdk4 and cdk2 activities, leading to complete cell cycle arrest in G1.. It is well documented that cGMP-generating reagents have an antimitogenic effect on SMC proliferation in vitro and in vivo.9 10 Because cAMP is also known to strongly suppress cell cycle transition in vascular SMCs,25 26 27 we sought to examine and delineate the molecular basis for cAMP and cGMP suppression of SMC proliferation. Interestingly, SMCs treated with cGMP do not enter the S phase 24 hours after PDGF stimulation, whereas at 30 hours, a significant portion of the cells travel to the S phase. This result suggests that cGMP delays, but does not block, the G1/S transition, probably through the prolongation of G1. In contrast, ...
In this study, we aimed to study the gene expression patterns at single cell level across the different cell cycle stages in mESC. We performed single cell RNA-Seq experiment on mESC that were stained with Hoechst 33342 and Flow cytometry sorted for G1, S and G2M stages of cell cycle. Single cell RNA-Seq was performed using Fluidigm C1 system and libraries were generated using Nextera XT (Illumina) kit.
Following a pathological insult, the adult mammalian heart undergoes hypertrophic growth and remodeling of the extracellular matrix. Although a small subpopulation of cardiomyocytes can reenter the cell cycle following cardiac injury, the myocardium is largely thought to be incapable of significant regeneration. Periostin, an extracellular matrix protein, has recently been proposed to induce reentry of differentiated cardiomyocytes back into the cell cycle and promote meaningful repair following myocardial infarction. Here, we show that although periostin is induced in the heart following injury, it does not stimulate DNA synthesis, mitosis, or cytokinesis of cardiomyocytes in vitro or in vivo. Mice lacking the gene encoding periostin and mice with inducible overexpression of full-length periostin were analyzed at baseline and after myocardial infarction. There was no difference in heart size or a change in cardiomyocyte number in either periostin transgenic or gene-targeted mice at baseline.
6. at which phase of meiosis the two cells each with separate sister chromatids move towards opposite polesat which phase of meiosis the two cells each with separate sister chromatids move towards opposite ...
Mitosis and meiosis are certainly among the most spectacular events in all of biology. These processes are brought about by protein kinase complexes consisting of the cyclin-dependent kinase CDK1 (also called Cdc2) and a mitotic cyclin (in animals, an A-type cyclin or a B-type cyclin). The abrupt activation of cyclin-CDK1 at the onset of mitosis, and the abrupt inactivation of cyclin-CDK1 at the metaphase/anaphase transition near the end of mitosis, constitute the climax of the cell cycle and result in the division of one cell into two. In some circumstances, the eukaryotic cell cycle can be best described as a succession of contingent events. For example, in most somatic cells in culture, cell growth is followed by DNA replication, then more cell growth, then mitotic entry and chromosome congression, then sister chromatid separation and mitotic exit. Entry into a new phase of the cell cycle may depend upon the successful completion of some important event in the previous phase. E.g., the cell ...
Mitosis and meiosis are certainly among the most spectacular events in all of biology. These processes are brought about by protein kinase complexes consisting of the cyclin-dependent kinase CDK1 (also called Cdc2) and a mitotic cyclin (in animals, an A-type cyclin or a B-type cyclin). The abrupt activation of cyclin-CDK1 at the onset of mitosis, and the abrupt inactivation of cyclin-CDK1 at the metaphase/anaphase transition near the end of mitosis, constitute the climax of the cell cycle and result in the division of one cell into two. In some circumstances, the eukaryotic cell cycle can be best described as a succession of contingent events. For example, in most somatic cells in culture, cell growth is followed by DNA replication, then more cell growth, then mitotic entry and chromosome congression, then sister chromatid separation and mitotic exit. Entry into a new phase of the cell cycle may depend upon the successful completion of some important event in the previous phase. E.g., the cell ...
Great news, we have finally launched a website devoted to the Australian Cell Cycle community ! This site will serve as a hub for all the amazing cell cycle research that is performed in Australia. In addition, we will also be rebooting the Australian Cell Cycle Workshop (ACCW), with a tentative date of early April…
海词词典,最权威的学习词典,专业出版cell cycle proteims是什么意思,cell cycle proteims的用法,cell cycle proteims翻译和读音等详细讲解。海词词典:学习变容易,记忆很深刻。
Members of the AP‐1 transcription complex were shown to be important regulators of the G0-G1 transition of the cell cycle. In the present study, we investigated the role of some of these genes in normally cycling cells. Combining flow cytometry measurements, immunofluorescence staining and Western blotting experiments, we showed that c‐Jun protein levels varied little during the cell cycle. In contrast, JunB displayed a highly heterogeneous distribution, especially in the G2/M and G1 phases. Immuno fluorescence microscopy revealed that the level of JunB protein was low in mitotic cells. Using synchronized cells, we were able to define more precisely the timing of the decrease in JunB abundance and showed that it was correlated with an increase in its apparent molecular weight, due to phosphorylation.. We investigated which kinase may be responsible for JunB phoshorylation. JunB contains a JNK docking site, but lacks serine residues analogous to the phosphorylated sites in c‐Jun. While ...
From http://en.wikipedia.org/wiki/Cell_cycle) The cell cycle is the series of events that takes place in a cell leading to its division and duplication (replication). Regulation of the cell cycle involves processes crucial to the survival of a cell, including the detection and repair of genetic damage as well as the prevention of uncontrolled cell division. Two key classes of regulatory molecules, cyclins and cyclin-dependent kinases (CDKs), determine a cells progress through the cell cycle ...
The focus of this study was to identify signaling pathways and potential therapeutic agents that would allow reproducible stimulation of DNA synthesis, cell cycle progression, and proliferation in human β-cells. We found that glucose, mTOR activity, and inhibition of GSK-3 together stimulated these regenerative processes in a highly reproducible manner in adult human β-cells regardless of sex, age, BMI, or isolation center.. Both LiCl and 1-Akp significantly enhanced DNA synthesis above that of 8 mmol/l glucose, and LiCl-mediated DNA synthesis was more sensitive to rapamycin than 1-Akp. This finding suggested that a component of 1-Akp-stimulated DNA synthesis in human islets is mTOR independent. Although lithium at higher concentrations decreased DNA synthesis in human islets, this did not appear to be due to apoptosis because cell cycle analysis (Fig. 3A and B) failed to detect a significant degree of apoptosis under similar conditions. Mussmann et al. (18) reported that lithium produces ...
A salt compound of a curcumin analogue, potassium pentagamavunon-0 (K PGV-0) has been synthesized to improve solubility of pentagamavunon-0 which has been proven to have anti-proliferative effects on several cancer cells. The purpose of this study was to investigate cytotoxic activity and metastasis inhibition by K PGV- 0 alone and in combination with achemotherapeutic agent, doxorubicin (dox), in breast cancer cells. Based on MTT assay analysis, K PGV-0 showed cytotoxic activity in T47D and 4T1 cell lines with IC50 values of 94.9 M and 49.00.2 M, respectively. In general, K PGV-0dox demonstrated synergistic effects and decreased cell viability up to 84.7% in T47D cells and 62.6% in 4T1 cells. Cell cycle modulation and apoptosis induction were examined by flow cytometry. K PGV-0 and K PGV-0dox caused cell accumulation in G2/M phase and apoptosis induction. Regarding cancer metastasis, while K PGV-0 alone did not show any inhibition of 4T1 cell migration, K PGV-0dox exerted inhibition. K PGV-0 and its
Cell Cycle includes many processes necessary for successful self-replication, and consists of DNA synthesis (S) and mitosis (M) phases separated by gap phases in the order G1-S-G2-M. S phase and M phase are usually separated by gap phases called G1 and G2, when cell-cycle progression can be regulated by various intracellular and extracellular signals. In order to move from one phase of its life cycle to the next, a cell must pass through numerous checkpoints. At each checkpoint, specialized proteins determine whether the necessary conditions exist. Progression through G1 phase is controlled by pRB proteins, and phosphorylation of pRB proteins by CDKs releases E2F factors, promoting the transition to S phase. The G2/M transition that commits cells to division is a default consequence of initiating the cell cycle at the G1/S transition, many proteins, such Wee1, PLK1 and cdc25, is involved the regulation of this process. The best-understood checkpoints are those activated by DNA damage and ...
Replication protein A (RPA) is a single-strand DNA-binding protein with essential roles in DNA replication, recombination and repair. RPA is necessary for the formation of the preincision complex which is required for proper incision of damaged DNA nucleotides during DNA repair. We have previously identified small molecule inhibitors (SMIs) with the ability to disrupt RPA binding activity to ssDNA. Further characterization of these RPA inhibitors was assessed using both lung and ovarian cancer cell lines. Lung cancer cell lines demonstrated increased apoptotic cell death following treatment with the SMI MCI13E, with IC50 values of ~5 µM. The A2780 ovarian cancer cell line and the p53-null lung cancer cell line H1299 were particularly sensitive to MCI13E treatment with IC50 values below 3 µM. Furthermore, a cell cycle effect was observed in lung cancer cell lines which resulted in a lengthening of either G1 or S-phases of the cell cycle following single agent treatment. Sequential treatment ...
Video articles in JoVE about retinoblastoma protein include In Vivo Detection and Analysis of Rb Protein SUMOylation in Human Cells, Workflow for High-content, Individual Cell Quantification of Fluorescent Markers from Universal Microscope Data, Supported by Open Source Software, Analysis of Cell Cycle Position in Mammalian Cells, Induction of Protein Deletion Through In Utero Electroporation to Define Deficits in Neuronal Migration in Transgenic Models, Whole Mount Dissection and Immunofluorescence of the Adult Mouse Cochlea, In vitro Coculture Assay to Assess Pathogen Induced Neutrophil Trans-epithelial Migration, An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus, A Protein Preparation Method for the High-throughput Identification of Proteins Interacting with a Nuclear Cofactor Using LC-MS/MS Analysis, Genome-wide Analysis using ChIP to Identify Isoform-specific Gene Targets, Assessing Replication and Beta Cell Function in Adenovirally-transduced
The prospect of exploiting mathematical and computational models to gain insight into the influence of scheduling on cancer chemotherapeutic effectiveness is increasingly being considered. However, the question of whether such models are robust to the inclusion of additional tumour biology is relatively unexplored. In this paper, we consider a common strategy for improving protocol scheduling that has foundations in mathematical modelling, namely the concept of dose densification, whereby rest phases between drug administrations are reduced. To maintain a manageable scope in our studies, we focus on a single cell cycle phase-specific agent with uncomplicated pharmacokinetics, as motivated by 5-Fluorouracil-based adjuvant treatments of liver micrometastases. In particular, we explore predictions of the effectiveness of dose densification and other escalations of the protocol scheduling when the influence of toxicity constraints, cell cycle phase specificity and the evolution of drug resistance ...
Early studies in lower Eukaryotes have defined a role for the members of the NimA related kinase (Nek) family of protein kinases in cell cycle control. Expansion of the Nek family throughout evolution has been accompanied by their broader involvement in checkpoint regulation and cilia biology. Moreover, mutations of Nek family members have been identified as drivers behind the development of ciliopathies and cancer. Recent advances in studying the physiological roles of Nek family members utilizing mouse genetics and RNAi-mediated knockdown are revealing intricate associations of Nek family members with fundamental biological processes. Here, we aim to provide a comprehensive account of our understanding of Nek kinase biology and their involvement in cell cycle, checkpoint control and cancer.
Punctuated evolution and transitional hybrid network in an ancestral cell cycle of fungi Edgar M. Medina, Jonathan J. Turner, Jan M. Skotheim, Nicolas E. Buchler bioRxiv doi: http://dx.doi.org/10.1101/038372 Although cell cycle control is an ancient, conserved, and essential process, some core animal and fungal cell cycle regulators share no more sequence identity than non-homologous proteins.…
CDC6 is conserved during evolution and is essential and limiting for the initiation of eukaryotic DNA replication. Human CDC6 activity is regulated by periodic transcription and CDK-regulated subcellular localization. Here, we show that, in addition to being absent from nonproliferating cells, CDC6 is targeted for ubiquitin-mediated proteolysis by the anaphase promoting complex (APC)/cyclosome in G(1). A combination of point mutations in the destruction box and KEN-box motifs in CDC6 stabilizes the protein in G(1) and in quiescent cells. Furthermore, APC, in association with CDH1, ubiquitinates CDC6 in vitro, and both APC and CDH1 are required and limiting for CDC6 proteolysis in vivo. Although a stable mutant of CDC6 is biologically active, overexpression of this mutant or wild-type CDC6 is not sufficient to induce multiple rounds of DNA replication in the same cell cycle. The APC-CDH1-dependent proteolysis of CDC6 in early G(1) and in quiescent cells suggests that this process is part of a ...
Cell cycle in somatic cells vs. ESCs. (a) Cell cycle regulation in somatic cells: mitogen signaling through MAPK path
Checkpoints are activated through the cell cycle by a series of sensors that recognize DNA damage of cellular abnormalities. If a sensor detects the presence of a defect, it triggers a response that temporarily holds further cell cycle progress so repairs can be made. This is important because undergoing division with genetic damage runs the risk of the cells becoming cancerous. If the DNA is damaged beyond repair, the checkpoint mechanism can transmit a signal that leads to the death of the hazardous cell. The spindle checkpoint operates between metaphase and anaphase. It comes to life when a chromosome fails to align properly at the metaphase plate like in the experiment mentioned above ...
Cell proliferation is a crucial cellular process which influences development. In plants, meristems are formed by actively proliferating cells, in which the main expression of proliferation is the existence of a cell division cycle. Many cell activities are influenced by the cell proliferation status and cell cycle progression, among them ribosome biogenesis, which is morphologically expressed as the nucleolus. The connection is established through nucleolar proteins, which regulate the synthesis and processing of preribosomal precursors and, at the same time, are targets of various cell cycle regulators, such as certain kinases. Nucleolin is one of these nucleolar proteins, whose level increases with cell proliferation and depends on the cell cycle stages. Not only the levels, but also other important features of the protein, such as its distribution in situ in the nucleolus, its phosphorylation and its physiological degradation, depend on these parameters. Furthermore, since the nucleolar ...
Within this site you can view figures from the papers, supplementary data, and interactively explore the cell cycle dataset. In addition, raw data and processed data are available for download.. ...
View Notes - bild lecture week 5.2 from BIOLOGY bild 1 at UCSD. Review: Monday. Skip chapter 11. Review: PSII PSI NADPH Mitosis and Cell Cycle 1.) Cell Cycle a. Alternates between interphase and
Equity mission statement The Australian Cell Cycle Meeting aims to promote the highest standard of research in the areas of cell cycle, DNA damage response and telomeres. To this end, the Australian Cell Cycle Meeting endeavours to foster a culture of inclusion and equity in all of its activities, including conference organisation, conference participation, and…
A ready-to-use reverse transfection format RNAi screening library targeting human cell cycle regulation genes. Just resuspend pre-dispensed siRNA, and add cells. Optimization plates are available.
In all living organisms, the phosphorylation of proteins modulates various aspects of their functionalities. In eukaryotes, protein phosphorylation plays a key role in cell signaling, gene expression, and differentiation. Protein phosphorylation is also involved in the global control of DNA replication during the cell cycle, as well as in the mechanisms that cope with stress-induced replication blocks. Similar to eukaryotes, bacteria use Hanks-type kinases and phosphatases for signal transduction, and protein phosphorylation is involved in numerous cellular processes. However, it remains unclear whether protein phosphorylation in bacteria can also regulate the activity of proteins involved in DNA-mediated processes such as DNA replication or repair. Accumulating evidence supported by functional and biochemical studies suggests that phospho-regulatory mechanisms also take place during the bacterial cell cycle. Recent phosphoproteomics and interactomics studies identified numerous phosphoproteins
But, if genes like Myc and E1A can induce ARF and p53 to trigger growth arrest or cell death, how can these same genes immortalize normal cells and collaborate with oncogenic Ras to transform them? A reasonable hypothesis is that Myc and E1A overexpression, by inducing both cell proliferation and compensating p53-dependent apoptosis, selects for resistant cells that have sustained mutations in the ARF-Mdm2-p53 pathway and that can now be transformed by oncogenic Ras alone. To test this idea, primary MEFs were infected with a high titer Myc retrovirus, and Myc-induced apoptosis was enforced by depriving the infected cells of serum-containing survival factors. Rare surviving cells were then recloned, expanded as colonies, and genotyped for p53 mutations and/or ARF loss. Strikingly, all such colonies lost the function of p53 or ARF but not both (93) . In short, ARF normally acts to protect cells from Myc overexpression by facilitating Myc-induced, p53-dependent apoptosis. Cells corrupted in the ...
Translational control enables faster transitions and fine-tuning of archetypal and specialized cell cycles [20]. Accumulation of translationally controlled cell cycle regulators is rapid, because time-consuming transcription and mRNA processing have already occurred. For many key cell cycle regulators, translational control represents an additional mechanism to precisely adjust their abundance, working in concert with transcriptional regulation, control of mRNA stability and ubiquitin-mediated degradation [6-8]. It remains to be discovered how all these different steps of gene-expression control are integrated to produce optimal levels of cell cycle players.. Although some progress has been made in understanding 5′ UTR-mediated translational control during archetypal cell cycle progression, the contribution of the 3′ UTR and 3′ UTR-binding proteins is largely unexplored. RNA-affinity chromatography could lead to identification of additional RNA-binding proteins interacting with 5′ UTRs ...
Cell cycle analysis is commonly used in biomedical research studies and clinical diagnosis. It helps in distinguishing cells that are in different phases of cell cycle and used to determine the cellular response to biological stimulations and various drug
Genome maintenance is required for cellular viability, and failure to preserve genomic integrity is associated with an increased risk of diseases, such as cancer. To ensure genomic stability, cells have checkpoints that control cell cycle progression in the event of DNA damage or incomplete DNA replication. The DNA replication checkpoint is regulated by the ATR-CHK1 pathway that stabilizes stalled replication forks and prevents their collapse into DNA double-strand breaks (DSBs). Two distinct models have been proposed to explain how ATR stabilizes stalled forks: 1) through local modulation of fork remodelers, such as SMARCAL1 inhibition, and 2) through inhibition of CDK-dependent pathways, such as inhibition of the AURKA-PLK1 pathway, which prevent cell cycle progression. However, it remains unclear which stabilization function is essential for fork stability and whether specific sites in the genome depend on one function over the other. In an effort to test if an essential part of fork ...
SLBP levels are controlled by cell-cycle proteins, causing SLBP to accumulate as cells enter S phase and degrade as cells leave ... Link between cell-cycle control machinery and histone synthesis[edit]. Nuclear protein Ataxia-Telangiectasia (NPAT), also known ... Masumoto H, Hawke D, Kobayashi R, Verreault A (Jul 2005). "A role for cell-cycle-regulated histone H3 lysine 56 acetylation in ... "Cell. 148 (4): 664-78. doi:10.1016/j.cell.2011.12.029. PMC 3281992. PMID 22325148.. ...
chromosome organization involved in meiotic cell cycle. • mitotic recombination. • protein homooligomerization. • response to ... Esophageal squamous cell cancer. Over-expression. 47%. Immunohistochemistry. [24]. Renal cell carcinoma. Under-expression. 100% ... "MicroRNAs down-regulate homologous recombination in the G1 phase of cycling cells to maintain genomic stability". Elife. 3: ... "Association of BRCA1 with Rad51 in mitotic and meiotic cells". Cell. 88 (2): 265-75. doi:10.1016/s0092-8674(00)81847-4. PMID ...
Downstream effects of this include regulation of gene expression and the cell cycle. The role of PI3K has been investigated by ... PDGF[1][2] is a potent mitogen for cells of mesenchymal origin, including fibroblasts, smooth muscle cells and glial cells. In ... "Cell Death and Control of Cell Survival in the Oligodendrocyte Lineage". Cell. 70 (1): 31-46. doi:10.1016/0092-8674(92)90531-G ... vascular smooth muscle cells and mesenchymal stem cells as well as chemotaxis, the directed migration, of mesenchymal cells. ...
regulation of cell cycle. • cell division. • negative regulation of cell cycle arrest. • protein phosphorylation. • lens ... cell cycle. • positive regulation of G2/M transition of mitotic cell cycle. • response to toxic substance. • positive ... and CDK5 cell cycle kinase genes". Cytogenet. Cell Genet. 66 (1): 72-4. doi:10.1159/000133669. PMID 8275715.. ... "Down-regulation of p21WAF1/CIP1 or p27Kip1 abrogates antiestrogen-mediated cell cycle arrest in human breast cancer cells". ...
Doonan, J.; Hunt, T. (1996). "Cell cycle. Why don't plants get cancer?". Nature. 380: 481-2. doi:10.1038/380481a0. PMID 8606760 ... Jamin, M, H Raveh-Barak, B Podbilewicz, FA Rey (2014) "Structural basis of eukaryotic cell-cell fusion" (Cell, Volume 157, ... Multicellular organisms arise in various ways, for example by cell division or by aggregation of many single cells.[2] Colonial ... In some multicellular groups, which are called Weismannists, a separation between a sterile somatic cell line and a germ cell ...
Cells may also temporarily or permanently leave the cell cycle and enter G0 phase to stop dividing. This can occur when cells ... Related cell processes[edit]. Cell rounding[edit]. Cell shape changes through mitosis for a typical animal cell cultured on a ... The Cell-Cycle Ontology. *WormWeb.org: Interactive Visualization of the C. elegans Cell Lineage - Visualize the entire cell ... Onion (Allium) cells in different phases of the cell cycle enlarged 800 diameters.. a. non-dividing cells. b. nuclei preparing ...
"Cell Cycle. 10 (15): 2549-60. doi:10.4161/cc.10.15.16531. PMC 3180193 . PMID 21701264.. ... doi:10.1016/j.cell.2016.02.063. PMID 27087445.. *^ Garg A, Xing C (2014). "De novo heterozygous FBN1 mutations in the extreme C ... "J Cell Biol. 199 (1): 9-13. doi:10.1083/jcb.201207072. PMC 3461511 . PMID 23027899.. ... "J Cell Biol. 176 (7): 1061-71. doi:10.1083/jcb.200611026. PMC 2064089 . PMID 17371835.. ...
Cell Cycle. 5 (10): 1080-4. doi:10.4161/cc.5.10.2741. PMID 16687933.. ... Collins FS, Rossant J, Wurst W (January 2007). "A mouse for all reasons". Cell. 128 (1): 9-13. doi:10.1016/j.cell.2006.12.018. ... "The Plant Cell. 19 (3): 1023-38. doi:10.1105/tpc.106.045427. PMC 1867357. PMID 17351118.. ... The protein is present in bacteria and in the chloroplasts[2] and mitochondria[7] of some eukaryotic cells. In eukaryotes and ...
cell division. • protein phosphorylation. • cell cycle. • G2/M transition of mitotic cell cycle. • regulation of actin ... neuronal cell body. • plasma membrane. • Golgi cisterna. • cleavage furrow. • midbody. • cell nucleus. • cytoskeleton. • actin ... mitotic cell cycle. • liver development. • peptidyl-threonine phosphorylation. • cortical actin cytoskeleton organization. • ... Liu H, Di Cunto F, Imarisio S, Reid LM (Jan 2003). "Citron kinase is a cell cycle-dependent, nuclear protein required for G2/M ...
positive regulation of cell migration. • neuron cell-cell adhesion. • nervous system development. • neuron maturation. • ... regulation of cell adhesion. • lymphocyte migration into lymphoid organs. • cell adhesion. • positive regulation of gene ... neural crest cell migration. • neuron differentiation. • positive regulation of cell size. • positive regulation of neuron ... neuronal cell body. • dendrite. • early endosome. • membrane raft. • endosome membrane. • plasma membrane. • cytosol. • plasma ...
Levine A, Brivanlou A (2006). "GDF3 at the crossroads of TGF-beta signaling". Cell Cycle. 5 (10): 1069-73. doi:10.4161/cc.5.10. ... Levine A, Brivanlou A (2006). "GDF3, a BMP inhibitor, regulates cell fate in stem cells and early embryos". Development. 133 (2 ... Kim J, Wu H, Lander A, Lyons K, Matzuk M, Calof A (2005). "GDF11 controls the timing of progenitor cell competence in ... Francis-West P, Parish J, Lee K, Archer C (1999). "BMP/GDF-signalling interactions during synovial joint development". Cell ...
traversing start control point of mitotic cell cycle. • negative regulation of cell cycle arrest. • protein ubiquitination. • ... positive regulation of cell cycle. • ventricular septum development. • positive regulation of protein export from nucleus. • ... positive regulation of mitotic cell cycle. • heart development. • cellular response to alkaloid. • cellular response to vitamin ... Ivanchuk SM, Mondal S, Rutka JT (June 2008). "p14ARF interacts with DAXX: effects on HDM2 and p53". Cell Cycle. 7 (12): 1836-50 ...
Inhibition of the Citric Acid Cycle forces the cell to create ATP glycolytically in order to generate its required energy. The ... "Cell-permeating alpha-ketoglutarate derivatives alleviate pseudohypoxia in succinate dehydrogenase-deficient cells". Mol. Cell ... Normal α-ketoglutarate does not permeate cell walls efficiently, and it is necessary to create a cell permeating derivative (e. ... Paraganglionic tissue is derived from the neural crest cells present in an embryo. Abdominal extra-adrenal paraganglionic cells ...
cell cycle. • response to radiation. • DNA repair. • sister chromatid cohesion. • response to DNA damage checkpoint signaling. ... Wong RW (May 2010). "An update on cohesin function as a 'molecular glue' on chromosomes and spindles". Cell Cycle. 9 (9): 1754- ... "Cell. 171 (2): 305-320.e24. doi:10.1016/j.cell.2017.09.026. PMC 5846482. PMID 28985562.. ... In addition to entrapping DNA to ensure proper chromosome segregation during the cell cycle, SMC1A, as a component of cohesin, ...
cell cycle arrest. • Bergmann glial cell differentiation. • peptidyl-tyrosine phosphorylation. • regulation of Golgi ... regulation of mitotic cell cycle. • regulation of apoptotic process. • protein phosphorylation. • peptidyl-threonine ... 2006). "ERK and beyond: insights from B-Raf and Raf-1 conditional knockouts". Cell Cycle. 5 (14): 1514-8. doi:10.4161/cc.5.14. ... negative regulation of cell proliferation. • thymus development. • cell motility. • negative regulation of gene expression. • ...
Cell Cycle. 7 (16): 2601-8. doi:10.4161/cc.7.16.6541. PMID 18719372.. ... neuronal cell fate, cell death, proliferation, fat storage, haematopoietic cell fate, insulin secretion.[17] ... RNA silencing is the mechanism that our cells (and cells from all kingdoms) use to fight RNA viruses and transposons (which ... "Both natural and designed micro RNAs can inhibit the expression of cognate mRNAs when expressed in human cells". Molecular Cell ...
cell cycle arrest. • positive regulation of response to DNA damage stimulus. • positive regulation of cell proliferation. • ... "Cell-cycle control of c-myc but not c-ras expression is lost following chemical transformation". Cell. 36 (2): 241-7. PMID ... G1/S transition of mitotic cell cycle. • regulation of transcription from RNA polymerase II promoter. • protein ... Taira T, Sawai M, Ikeda M, Tamai K, Iguchi-Ariga SM, Ariga H (August 1999). "Cell cycle-dependent switch of up-and down- ...
"Role of Fanconi DNA repair pathway in neural stem cell homeostasis". Cell Cycle. 7 (13): 1911-5. doi:10.4161/cc.7.13.6235. PMID ... Cell. 7 (2): 249-62. doi:10.1016/s1097-2765(01)00173-3. PMID 11239454. Yang Y, Kuang Y, Montes De Oca R, Hays T, Moreau L, Lu N ... Cell. Biol. 19 (7): 4866-73. doi:10.1128/mcb.19.7.4866. PMC 84285 . PMID 10373536. Park SJ, Ciccone SL, Beck BD, Hwang B, Freie ... Cell. Biol. 19 (7): 4866-73. doi:10.1128/mcb.19.7.4866. PMC 84285 . PMID 10373536. Jelesko JG, Harper R, Furuya M, Gruissem W ( ...
Valastyan S, Weinberg RA (2010). "miR-31: A crucial overseer of tumor metastasis and other emerging roles". Cell Cycle. 9 (11 ... There has also been observed a strong encapsulation of tumour cells expressing miR-31, as well as a reduced cell survival rate ... Conversely, in gastric cancer miR-31 levels have been found to be significantly lower in tumour cells relative to healthy cells ... Cancer cell lines with an inactive p53 pathway show a vulnerability to miR-31 overexpression, whilst there is resistance to ...
"Cell Cycle. 4 (11): 1510-4. doi:10.4161/cc.4.11.2187. PMC 1402358. PMID 16294017.. ... host cell. • protein complex. • macromolecular complex. • Ribonucleoprotein. • intracellular. • cell. Biological process. • ... Kudo N, Khochbin S, Nishi K, Kitano K, Yanagida M, Yoshida M, Horinouchi S (Dec 1997). "Molecular cloning and cell cycle- ... Görlich D, Kutay U (1999). "Transport between the cell nucleus and the cytoplasm". Annu. Rev. Cell Dev. Biol. 15 (1): 607-60. ...
A G0-G1 cell-cycle blockage can be the consequence of inactivation of mTOR in hypoxia-activated pericytes and endothelial cells ... That leads to late blockage of G1/S cell cycle. Rapamycin has shown to induce cancer cell death by stimulating autophagy or ... attenuate cell cycle progression, and inhibit angiogenesis in many cancer cell lines and also in human cancer. In fact they ... Ljungman, Mats (2007). "The transcription stress response". Cell Cycle. 6 (18): 2252-7. doi:10.4161/cc.6.18.4751. PMID 17700065 ...
Depletion of POLD1 can halt cell cycle at G1 and G2/M phases in human cells.[96] Cell cycle block in these phases typically ... the cell cycle element/cell cycle genes homology region (CDE/CHR), located downstream of the start site is important for POLD1 ... is degraded by ubiquitin ligases in response to DNA damage and during cell cycle progression". Cell Cycle. 13 (1): 23-31. doi: ... The POLD1 gene promoter is regulated via the cell cycle machinery and mRNA expression of POLD1 reaches a peak in late G1/S ...
Cell Cycle". 3 (8), s. 976-9, Aug 2004. PMID: 15254398. *↑ a b D. Bertwistle, M. Sugimoto, CJ. Sherr. Physical and functional ... Cell". 150 (2), s. 264-78, Jul 2012. DOI: 10.1016/j.cell.2012.06.023. PMID: 22817890. ... Cell". 128 (4), s. 683-92, Feb 2007. DOI: 10.1016/j.cell.2007.01.029. PMID: 17320506. ... Telomere shortening is associated with cell division in vitro and in vivo. „Exp Cell Res". 220 (1), s. 194-200, Sep 1995. DOI: ...
... for the study of fundamental cellular processes such as the cell cycle, DNA replication, recombination, cell division, and ... The bud continues to grow until it separates from the parent cell, forming a new cell.[42] The daughter cell produced during ... or daughter cell, is formed on the parent cell. The nucleus of the parent cell splits into a daughter nucleus and migrates into ... The dying yeast cells are then heated to complete their breakdown, after which the husks (yeast with thick cell walls that ...
... s can be divided into four classes based on their behavior in the cell cycle of vertebrate somatic cells and yeast cells ... Cell changes in the cell cycle like the assembly of mitotic spindles and alignment of sister-chromatids along the spindles are ... Baumann K (November 2013). "Cell cycle: Cyclin A corrections". Nature Reviews. Molecular Cell Biology. 14 (11): 692. doi: ... Cyclin is a family of proteins that control the progression of cells through the cell cycle by activating cyclin-dependent ...
... 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] ...
... mathematical model of DNA replication and cell division for the bacterium Caulobacter crescentus. ... Mutant cells provide valuable information about how individual components of the cell cycle control system affect the features ... Caulobacter normally undergoes a cell cycle that produces two different types of offspring: a motile "swarmer cell" with a ... Shenghua Li, Paul Brazhnik, Bruno Sobral, John J. Tyson (2009) Temporal controls of the asymmetric cell division cycle in ...
Cell Cycle Lab. Mitosis is the process of how eukaryotic cells divide and replicate. The process results in two cells with ... In most cells this is a short proportion of the overall cells existence, approximately 10%. The cell cycle is divided into ... The Mitotic index is a measure for the growth of a cell population or as the ratio between the number of cells in mitosis and ... How does the length of each portion of the cell cycle compare? ... cancerous cells divide at a higher rate, therefore, more cells ...
... and p53 confer specific gene expression profiles in mantle cell lymphoma Timothy C. Greiner, Chiranjib Dasgupta, Vincent V. Ho ...
Cell cycle, 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 (gap 1, or G1, stage), copies its DNA (synthesis, or S, stage), prepares to ... 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 ...
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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 ...
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 ...
... viruses typically require factors provided by the cells that they have infected. Subversion of the cellular machinery that ... To replicate their genomes in cells and generate new progeny, ... Cell cycle arrest may inhibit early cell death of infected ... Bagga S., Bouchard M.J. (2014) Cell Cycle Regulation During Viral Infection. In: Noguchi E., Gadaleta M. (eds) Cell Cycle ... Salvant BS, Fortunato EA, Spector DH (1998) Cell cycle dysregulation by human cytomegalovirus: influence of the cell cycle ...
Cell cycle. Stifled by inhibitions.. Peters G.. Comment on. *p15INK4B is a potential effector of TGF-beta-induced cell cycle ...
Growth during the cell cycle.. Mitchison JM1.. Author information. 1. Institute for Cell, Animal and Population Biology, ... Most of the bulk properties of cells show a continuous increase during the cell cycle, although the exact pattern of this ... cell size at division through successive cycles in a growing culture. It is a vital link coordinating cell growth with periodic ... During the cell cycle, major bulk parameters such as volume, dry mass, total protein, and total RNA double and such growth is a ...
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. https://www.news-medical.net/life-sciences/Histones-and-the-Cell-Cycle.aspx. ( ...
... 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, ...
Curr Opin Cell Biol. 2015 Apr;33:19-25. doi: 10.1016/j.ceb.2014.10.006. 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 ...
... asking at what point in the cell cycle did cells become "committed" to that cell cycle in the sense that alternative ... The principles underpinning cell-cycle control worked out in yeast cells had to be much the same in human cells. I experienced ... Murdoch knew all about the cell cycle, more about the fission yeast cell cycle than anyone else on the planet, but he was not a ... Hayles J, et al. (2013) A genome-wide resource of cell cycle and cell shape genes of fission yeast. Open Biol. 3:130053. ...
Curr Opin Cell Biol. 1994 Jun;6(3):451-9. Research Support, Non-U.S. Govt; Review ... cell cycle regulators and replication initiation proteins in G2; and genes needed for cell separation as cells enter G1. Early ... Cell cycle regulated transcription in yeast.. Koch C1, Nasmyth K.. Author information. 1. Institute of Molecular Pathology, ... At least four different classes of cell cycle regulated gene exist in yeast: G1 cyclins and DNA synthesis genes are expressed ...
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 ...
Cellcycle progression before commitment is dependent on growth and on cells reaching a minimum size. Cellcycle progression ... The Chlamydomonas cell cycle has a striking temporal and functional separation between cell growth and rapid cell division, ... Here, we review the current status of studies of the Chlamydomonas cell cycle. We begin with an overview of cell-cycle control ... Chlamydomonas multiple‐fission cell cycle. Schematic from left to right of one multiple‐fission cycle. Daughter cells grow ...
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 CellForCash.com, 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 sjumusic.stjohns.edu Mon Sep 26 14:30:49 EST 1994 *Previous message: ...
Regeneration potential of adult cardiac myocytes. [Cell Res. 2013]. *Cardiomyocyte cell cycle: Meis-ing something? [Cell Cycle ... Meis1 regulates postnatal cardiomyocyte cell cycle arrest.. Mahmoud AI#1, Kocabas F#1, Muralidhar SA#1, Kimura W1, Koura AS2, ... a, qRT-PCR showing increased expression of Meis1 at postnatal day 7 (P7), a time point that coincides with cell cycle arrest of ... Here we identify Meis1 as a critical regulator of the cardiomyocyte cell cycle. Meis1 deletion in mouse cardiomyocytes was ...
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 ...
  • By careful examination of the large amount of experimental information available about the genes, proteins and biochemical reactions involved in regulating the cell division of C. crescentus , we have developed a good understanding of the mechanism of cell division in this organism and a realistic, quantitative mathematical model of the molecular machinery that oversees Caulobacter's cell division cycle," said John Tyson. (eurekalert.org)
  • This regulatory core comprises three key proteins - DnaA, GcrA, and CtrA - that act as control points or master switches for DNA replication and cell division. (eurekalert.org)
  • The new math model allows scientists to investigate how these proteins vary with time and their link to physiological events in both stalked and swarmer cells. (eurekalert.org)
  • They were able to show in simulations that the model accurately describes how the different proteins change in quantity during the cell division cycle. (eurekalert.org)
  • Blacksburg, Va. - Scientists from the Department of Biological Sciences and the Virginia Bioinformatics Institute (VBI) at Virginia Tech have developed a quantitative, mathematical model of DNA replication and cell division for the bacterium Caulobacter crescentus . (eurekalert.org)
  • Conveying instructions for DNA replication and cell division has profound consequences for a cell and needs to be done with considerable accuracy and precision and that's one of the reasons why we want to be able to model the process. (eurekalert.org)
  • Tyson added: "We have been able to establish a wiring diagram that maps the essential regulatory steps for DNA replication and cell division in Caulobacter in a way that is similar to how you would define a computer process. (eurekalert.org)
  • Caulobacter normally undergoes a cell cycle that produces two different types of offspring: a motile "swarmer cell" with a flagellum, a slender thread-like structure that allows the bacterium to swim, and an immobile "sessile stalked cell" that lacks a flagellum. (eurekalert.org)
  • The article "Temporal controls of the asymmetric cell division cycle in Caulobacter crescentus" is by Genetics, Bioinformatics, and Computational Biology graduate student Shenghua Li, research scientist Paul Brazhnik, Professor and Director of VBI's Cyberinfrastructure Group Bruno Sobral, and University Distinguished Professor of Biological Sciences John Tyson. (eurekalert.org)
  • The two cell types undergo different development programs but share the same core molecular regulatory system that controls whether the cell commits to a new round of DNA synthesis and to the cell division process. (eurekalert.org)
  • For example, the math model predicts that if the master regulator CtrA cannot be properly phosphorylated, which is a key step in the activation of CtrA, then the cell replicates its DNA but cannot divide. (eurekalert.org)
  • With the model in place, the researchers confirmed that it correctly represents the sequence of physiological events that take place during cell division. (eurekalert.org)
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