Cyclin dependent kinase inhibitor p57. Medical search

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.

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.

Protein kinases that control cell cycle progression in all eukaryotes and require physical association with CYCLINS to achieve full enzymatic activity. Cyclin-dependent kinases are regulated by phosphorylation and dephosphorylation events.

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.

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.

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.

The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.

Proteins that are normally involved in holding cellular growth in check. Deficiencies or abnormalities in these proteins may lead to unregulated cell growth and tumor development.

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.

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 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.

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.

A 50-kDa protein that complexes with CYCLIN-DEPENDENT KINASE 2 in the late G1 phase of the cell cycle.

All of the processes involved in increasing CELL NUMBER including CELL DIVISION.

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.

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.

One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.

A 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.

A cell line derived from cultured tumor cells.

Agents that inhibit PROTEIN KINASES.

A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.

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.

A serine-threonine kinase that plays important roles in CELL DIFFERENTIATION; CELL MIGRATION; and CELL DEATH of NERVE CELLS. It is closely related to other CYCLIN-DEPENDENT KINASES but does not seem to participate in CELL CYCLE regulation.

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.

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.

Phosphoprotein with protein kinase activity that functions in the G2/M phase transition of the CELL CYCLE. It is the catalytic subunit of the MATURATION-PROMOTING FACTOR and complexes with both CYCLIN A and CYCLIN B in mammalian cells. The maximal activity of cyclin-dependent kinase 1 is achieved when it is fully dephosphorylated.

A 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.

A cyclin subtype that binds to the CYCLIN-DEPENDENT KINASE 3 and CYCLIN-DEPENDENT KINASE 8. Cyclin C plays a dual role as a transcriptional regulator and a G1 phase CELL CYCLE regulator.

The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.

A broadly expressed type D cyclin. Experiments using KNOCKOUT MICE suggest a role for cyclin D3 in LYMPHOCYTE development.

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.

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.

The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.

Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.

Phase of the CELL CYCLE following G1 and preceding G2 when the entire DNA content of the nucleus is replicated. It is achieved by bidirectional replication at multiple sites along each chromosome.

A cyclin B subtype that colocalizes with MICROTUBULES during INTERPHASE and is transported into the CELL NUCLEUS at the end of the G2 PHASE.

An INK4 cyclin-dependent kinase inhibitor containing five ANKYRIN-LIKE REPEATS. Aberrant expression of this protein has been associated with deregulated EPITHELIAL CELL growth, organ enlargement, and a variety of NEOPLASMS.

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.

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.

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.

The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.

A 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.

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.

Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.

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.

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.

A cyclin A subtype primarily found in male GERM CELLS. It may play a role in the passage of SPERMATOCYTES into meiosis I.

A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein.

A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include ADENINE and GUANINE, constituents of nucleic acids, as well as many alkaloids such as CAFFEINE and THEOPHYLLINE. Uric acid is the metabolic end product of purine metabolism.

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.

Established cell cultures that have the potential to propagate indefinitely.

A type of CELL NUCLEUS division by means of which the two daughter nuclei normally receive identical complements of the number of CHROMOSOMES of the somatic cells of the species.

A cyclin subtype that is found associated with CYCLIN-DEPENDENT KINASE 5; cyclin G associated kinase, and PROTEIN PHOSPHATASE 2.

The period of the CELL CYCLE following DNA synthesis (S PHASE) and preceding M PHASE (cell division phase). The CHROMOSOMES are tetraploid in this point.

A 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.

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.

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.

An INK4 cyclin-dependent kinase inhibitor containing four ANKYRIN-LIKE REPEATS. INK4B is often inactivated by deletions, mutations, or hypermethylation in HEMATOLOGIC NEOPLASMS.

Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.

A cyclin 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.

An intracellular signaling system involving the MAP kinase cascades (three-membered protein kinase cascades). Various upstream activators, which act in response to extracellular stimuli, trigger the cascades by activating the first member of a cascade, MAP KINASE KINASE KINASES; (MAPKKKs). Activated MAPKKKs phosphorylate MITOGEN-ACTIVATED PROTEIN KINASE KINASES which in turn phosphorylate the MITOGEN-ACTIVATED PROTEIN KINASES; (MAPKs). The MAPKs then act on various downstream targets to affect gene expression. In mammals, there are several distinct MAP kinase pathways including the ERK (extracellular signal-regulated kinase) pathway, the SAPK/JNK (stress-activated protein kinase/c-jun kinase) pathway, and the p38 kinase pathway. There is some sharing of components among the pathways depending on which stimulus originates activation of the cascade.

A widely-expressed cyclin A subtype that functions during the G1/S and G2/M transitions of the CELL CYCLE.

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.

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.

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.

Transport proteins that carry specific substances in the blood or across cell membranes.

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.

Substances that inhibit or prevent the proliferation of NEOPLASMS.

Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.

The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.

Protein kinases that catalyze the PHOSPHORYLATION of TYROSINE residues in proteins with ATP or other nucleotides as phosphate donors.

A CALMODULIN-dependent enzyme that catalyzes the phosphorylation of proteins. This enzyme is also sometimes dependent on CALCIUM. A wide range of proteins can act as acceptor, including VIMENTIN; SYNAPSINS; GLYCOGEN SYNTHASE; MYOSIN LIGHT CHAINS; and the MICROTUBULE-ASSOCIATED PROTEINS. (From Enzyme Nomenclature, 1992, p277)

Histochemical localization of immunoreactive substances using labeled antibodies as reagents.

An INK4 cyclin-dependent kinase inhibitor containing five ANKYRIN REPEATS. Aberrant expression of this protein has been associated with TESTICULAR CANCER.

A family of structurally-related proteins that were originally identified by their ability to complex with cyclin proteins (CYCLINS). They share a common domain that binds specifically to F-BOX MOTIFS. They take part in SKP CULLIN F-BOX PROTEIN LIGASES, where they can bind to a variety of F-BOX PROTEINS.

A PROTEIN-TYROSINE KINASE family that was originally identified by homology to the Rous sarcoma virus ONCOGENE PROTEIN PP60(V-SRC). They interact with a variety of cell-surface receptors and participate in intracellular signal transduction pathways. Oncogenic forms of src-family kinases can occur through altered regulation or expression of the endogenous protein and by virally encoded src (v-src) genes.

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.

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.

Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.

The 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.

An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters.

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.

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.

The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.

Proteins and peptides that are involved in SIGNAL TRANSDUCTION within the cell. Included here are peptides and proteins that regulate the activity of TRANSCRIPTION FACTORS and cellular processes in response to signals from CELL SURFACE RECEPTORS. Intracellular signaling peptide and proteins may be part of an enzymatic signaling cascade or act through binding to and modifying the action of other signaling factors.

The 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.

A mitogen-activated protein kinase subfamily that regulates a variety of cellular processes including CELL GROWTH PROCESSES; CELL DIFFERENTIATION; APOPTOSIS; and cellular responses to INFLAMMATION. The P38 MAP kinases are regulated by CYTOKINE RECEPTORS and can be activated in response to bacterial pathogens.

Cell lines whose original growing procedure consisted being transferred (T) every 3 days and plated at 300,000 cells per plate (J Cell Biol 17:299-313, 1963). Lines have been developed using several different strains of mice. Tissues are usually fibroblasts derived from mouse embryos but other types and sources have been developed as well. The 3T3 lines are valuable in vitro host systems for oncogenic virus transformation studies, since 3T3 cells possess a high sensitivity to CONTACT INHIBITION.

A superfamily of PROTEIN-SERINE-THREONINE KINASES that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by MITOGEN-ACTIVATED PROTEIN KINASE KINASES, which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP KINASE KINASE KINASES).

A proline-directed serine/threonine protein kinase which mediates signal transduction from the cell surface to the nucleus. Activation of the enzyme by phosphorylation leads to its translocation into the nucleus where it acts upon specific transcription factors. p40 MAPK and p41 MAPK are isoforms.

A serine-threonine protein kinase family whose members are components in protein kinase cascades activated by diverse stimuli. These MAPK kinases phosphorylate MITOGEN-ACTIVATED PROTEIN KINASES and are themselves phosphorylated by MAP KINASE KINASE KINASES. JNK kinases (also known as SAPK kinases) are a subfamily.

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.

Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.

A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (CYTOSINE; THYMINE; and URACIL) and form the basic structure of the barbiturates.

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.

Elements of limited time intervals, contributing to particular results or situations.

A group of enzymes that are dependent on CYCLIC AMP and catalyze the phosphorylation of SERINE or THREONINE residues on proteins. Included under this category are two cyclic-AMP-dependent protein kinase subtypes, each of which is defined by its subunit composition.

Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.

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)

A 44-kDa extracellular signal-regulated MAP kinase that may play a role the initiation and regulation of MEIOSIS; MITOSIS; and postmitotic functions in differentiated cells. It phosphorylates a number of TRANSCRIPTION FACTORS; and MICROTUBULE-ASSOCIATED PROTEINS.

A protein-serine-threonine kinase that is activated by PHOSPHORYLATION in response to GROWTH FACTORS or INSULIN. It plays a major role in cell metabolism, growth, and survival as a core component of SIGNAL TRANSDUCTION. Three isoforms have been described in mammalian cells.

Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.

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.

BENZOIC ACID amides.

The rate dynamics in chemical or physical systems.

A subgroup of mitogen-activated protein kinases that activate TRANSCRIPTION FACTOR AP-1 via the phosphorylation of C-JUN PROTEINS. They are components of intracellular signaling pathways that regulate CELL PROLIFERATION; APOPTOSIS; and CELL DIFFERENTIATION.

Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.

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.

The relationship between the dose of an administered drug and the response of the organism to the drug.

A cyclin B subtype that colocalizes with GOLGI APPARATUS during INTERPHASE and is transported into the CELL NUCLEUS at the end of the G2 PHASE.

A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.

The parts of a macromolecule that directly participate in its specific combination with another molecule.

A group of phenyl benzopyrans named for having structures like FLAVONES.

p57(Kip2) is degraded through the proteasome in osteoblasts stimulated to proliferation by transforming growth factor beta1. (1/288)

Cyclin-dependent kinase inhibitory proteins are negative regulators of the cell cycle. Although all the cyclin-dependent kinase inhibitory proteins may be involved in cell cycle control during a differentiation process, only p57(Kip2) is shown to be essential for embryonic development. However, the role of p57 in the control of the cell cycle is poorly understood. Using osteoblasts derived from the calvaria of rat fetus, we show that p57 is accumulated in cells starved by low serum. Cyclin-dependent kinase 2 activity was suppressed in these cells with a significant amount bound to p57. Treatment of the cells with transforming growth factor beta1 dramatically reduced the amount of p57, resulting in an activation of cyclin-dependent kinase 2 activity and the stimulation of cell proliferation. The decrease in p57 was inhibited by treating the cells with proteasome inhibitors, Z-Leu-Leu-Leu-aldehyde or lactacystin, but not with Z-Leu-Leu-aldehyde, which is an inhibitor of calpain, indicating that p57 is degraded through the proteasome pathway. p57 was also shown to be ubiquitinated in vitro. Because transforming growth factor beta1 not only stimulates the growth but also inhibits the differentiation of the cells in this system, our results may suggest a possible involvement of p57 in the control of osteoblastic cell proliferation and differentiation. (+info)

Analysis of germline CDKN1C (p57KIP2) mutations in familial and sporadic Beckwith-Wiedemann syndrome (BWS) provides a novel genotype-phenotype correlation. (2/288)

Beckwith-Wiedemann syndrome (BWS) is a human imprinting disorder with a variable phenotype. The major features are anterior abdominal wall defects including exomphalos (omphalocele), pre- and postnatal overgrowth, and macroglossia. Additional less frequent complications include specific developmental defects and a predisposition to embryonal tumours. BWS is genetically heterogeneous and epigenetic changes in the IGF2/H19 genes resulting in overexpression of IGF2 have been implicated in many cases. Recently germline mutations in the cyclin dependent kinase inhibitor gene CDKN1C (p57KIP2) have been reported in a variable minority of BWS patients. We have investigated a large series of familial and sporadic BWS patients for evidence of CDKN1C mutations by direct gene sequencing. A total of 70 patients with classical BWS were investigated; 54 were sporadic with no evidence of UPD and 16 were familial from seven kindreds. Novel germline CDKN1C mutations were identified in five probands, 3/7 (43%) familial cases and 2/54 (4%) sporadic cases. There was no association between germline CDKN1C mutations and IGF2 or H19 epigenotype abnormalities. The clinical phenotype of 13 BWS patients with germline CDKN1C mutations was compared to that of BWS patients with other defined types of molecular pathology. This showed a significantly higher frequency of exomphalos in the CDKN1C mutation cases (11/13) than in patients with an imprinting centre defect (associated with biallelic IGF2 expression and H19 silencing) (0/5, p<0.005) or patients with uniparental disomy (0/9, p<0.005). However, there was no association between germline CDKN1C mutations and risk of embryonal tumours. No CDKN1C mutations were identified in six non-BWS patients with overgrowth and Wilms tumour. These findings (1) show that germline CDKN1C mutations are a frequent cause of familial but not sporadic BWS, (2) suggest that CDKN1C mutations probably cause BWS independently of changes in IGF2/H19 imprinting, (3) provide evidence that aspects of the BWS phenotype may be correlated with the involvement of specific imprinted genes, and (4) link genotype-phenotype relationships in BWS and the results of murine experimental models of BWS. (+info)

CDKN1C expression in Beckwith-Wiedemann syndrome patients with allele imbalance. (3/288)

In this study, we have examined CDKN1C expression in BWS patients with allele imbalance (AI) affecting the 11p15 region. Two of two informative patients with AI, attributable to mosaic paternal isodisomy, exhibited reduced levels of CDKN1C expression in the liver and kidney, respectively, relative to expression levels in the equivalent tissues in normal controls. Although overall expression was reduced, some expression from the paternally derived CDKN1C allele was evident, consistent with incomplete paternal imprinting of the gene. One patient showed evidence of maternal allele silencing in addition to AI. These findings show for the first time that CDKN1C expression is reduced in BWS patients with AI and suggest that CDKN1C haploinsufficiency contributes to the BWS phenotype in patients with mosaic paternal isodisomies of chromosome 11. (+info)

TGF-beta1-mediated hypertrophy involves inhibiting pRB phosphorylation by blocking activation of cyclin E kinase. (4/288)

When renal epithelial cells are exposed to epidermal growth factor-transforming growth factor-beta1 (EGF-TGF-beta1) the typical EGF-mediated hyperplastic growth response is converted to a hypertrophic growth response. Hypertrophy in this setting involves cell entrance into G(1), but arrest of cell cycle progression at the G(1)/S interface. Late G(1) arrest is mediated by retaining retinoblastoma protein (pRB) in its active, hypophosphorylated state. The present studies examine the mechanism by which pRB is retained in its active state. The results demonstrate that TGF-beta1-mediated conversion of hyperplasia to hypertrophy involves preventing activation of cdk2/cyclin E kinase but has no effect on cdk4(6)/cyclin D kinase activity. Preventing activation of cyclin E kinase is associated with 1) decreased abundance of cdk2/cyclin E complexes and 2) retention of p57(Kip2) in formed cdk2/cyclin E complexes. The development of hypertrophy does not involve regulation of either cdk2, cyclin E, or cdc25A protein abundances, or the abundance of p27(Kip1) or p21 in formed complexes. (+info)

Spatial and temporal expression of p57(KIP2) during murine lens development. (5/288)

The expression patterns of p57(KIP2), an important cyclin-dependent kinase inhibitor in the lens, is investigated. This study shows that the expression of p57 mRNA throughout lens morphogenesis and growth correlates with lens cell withdrawal from the cell cycle (shown by changing patterns of BrdU incorporation) and the onset of lens fibre differentiation (shown by beta-crystallin expression). p57 expression at the early stages of fibre differentiation make it a useful marker for the initiation of this process. (+info)

p57KIP2 expression and loss of heterozygosity during immortal conversion of cultured human mammary epithelial cells. (6/288)

We have uncovered a novel role for the cyclin-dependent kinase inhibitor, p57KIP2, during the immortalization of cultured human mammary epithelial cells (HMECs). HMECs immortalized after chemical carcinogen exposure initially expressed little or no telomerase activity, and their telomeres continued to shorten with passage. Cell populations whose mean terminal restriction fragment (TRF) length declined to < or = 3 kb exhibited slow heterogeneous growth and contained many nonproliferative cells. These conditionally immortal HMEC cultures accumulated large quantities of p57 protein. With continued passage, the conditionally immortal cell populations very gradually converted to a fully immortal phenotype of good uniform growth, expression of high levels of telomerase activity, and stabilization of telomere length. The fully immortal HMECs that grew well did not accumulate p57 in G0 or during the cell cycle. DNA and RNA analysis of mass populations and individual subclones of conditionally immortal HMEC line 184A1 showed that continued growth of conditionally immortal cells with critically short telomeres was repeatedly accompanied by loss of the expressed p57 allele and transient expression of the allele imprinted previously. Conditionally immortal 184A1 with mean TRF > 3 kb, infected with retroviruses containing the p57 gene, exhibited premature slow heterogeneous growth. Conversely, exogenous expression of human telomerase reverse transcriptase (hTERT), the catalytic subunit of telomerase, in 184A1 with mean TRF > 3 kb prevented both the slow heterogeneous growth phase and accumulation of p57 in cycling populations. These data indicate that in HMECs that have overcome replicative senescence, p57 may provide an additional barrier against indefinite proliferation. Overcoming p57-mediated growth inhibition in these cells may be crucial for acquisition of the unlimited growth potential thought to be critical for malignant progression. (+info)

A human p57(KIP2) transgene is not activated by passage through the maternal mouse germline. (7/288)

Genomic imprinting results in expression of some autosomal genes from one parental allele only. Human chromosome 11p15, and the syntenic region on mouse distal chromosome 7, contain several imprinted genes, including p57 (KIP2) ( CDKN1C ) and IGF2. These two genes, which are separated by >700 kb, are both implicated in the pathogenesis of Beckwith-Wiedemann syndrome. We have shown previously that an Igf2/H19 transgene is expressed appropriately and can imprint at ectopic chromosomal locations. To investigate the p57 (KIP2) region, we similarly tested the imprinting and function of a 38 kb human genomic fragment containing the p57 (KIP2) gene in transgenic mice. This transgene showed appropriate tissue-specific expression and transgene copy number-dependent expression at ectopic sites. However, the levels of expression are reminiscent of that found for the paternal allele in humans (10%). There was no change in expression levels when the transgene was inherited from the maternal germline. These results suggest that the cis -elements required for enhanced expression of the maternally inherited p57 (KIP2) allele lie at a distance from the gene. This finding has important implications for the role of this gene in the human disease, in particular with respect to the translocation breakpoints identified in some patients. (+info)

Mechanism for inactivation of the KIP family cyclin-dependent kinase inhibitor genes in gastric cancer cells. (8/288)

The mechanism for inactivation of the KIP family cyclin-dependent kinase inhibitor (CDKI) genes, the p21, p27, and p57 genes, in gastric cancer cells was tested by treating the cells with either the DNA demethylation agent, 5-aza-2'-deoxycytidine or the histone deacetylase inhibitor, n-butyric acid or trichostatin A. RNA expression of the gene was determined by reverse transcription PCR. The p21 gene was activated only by histone deacetylase inhibitor. The p57 gene was activated by histone deacetylase inhibitors in all of the gastric cancer cell lines and by 5-aza-2'-deoxycytidine in five of eight gastric cell lines. However, the p27 gene was not inactivated in gastric cancer cell lines. The methylation status of the promoter of the p21 and p57 genes was also tested by digestion with the methylation-sensitive restriction enzymes and a subsequent PCR. The promoter of the p21 gene has no methylation. The promoter of the p57 gene is, however, methylated in five of eight gastric cancer cell lines as expected from the result of the treatment with 5-aza-2'-deoxycytidine. Formation of the inactive chromatin through histone deacetylation seems to be the general mechanism for inactivation of both the p21 and the p57 genes in gastric cancer cells. Hypermethylation of promoter region seems to be an alternative pathway for inactivation of the p57 gene. (+info)

... (p57, Kip2), also known as CDKN1C, is a protein which in humans is encoded by the CDKN1C ... Cyclin-dependent kinase inhibitor 1C is a tight-binding inhibitor of several G1 cyclin/Cdk complexes and a negative regulator ... "Entrez Gene: CDKN1C cyclin-dependent kinase inhibitor 1C (p57, Kip2)". Matsuoka S, Edwards MC, Bai C, Parker S, Zhang P, ... Immuohistochemical stains for p57 can aid with the diagnosis of hydatidiform moles. Cyclin-dependent kinase inhibitor 1C has ...

https://en.wikipedia.org/wiki/Cyclin-dependent_kinase_inhibitor_1C

They are p15, p16, p18, p19, p21, p27, and p57. Russo AA, Jeffrey PD, Patten AK, Massagué J, Pavletich NP (July 1996). "Crystal ... A cyclin-dependent kinase inhibitor protein is a protein which inhibits the enzyme cyclin-dependent kinase (CDK). Several ... Seven cyclin-dependent kinase inhibitor proteins have thus far been identified. They are named by the small letter "p" followed ... Cyclin-Dependent+Kinase+Inhibitor+Proteins at the US National Library of Medicine Medical Subject Headings (MeSH) v t e ( ...

https://en.wikipedia.org/wiki/Cyclin-dependent_kinase_inhibitor_protein

Cyclin-dependent kinase inhibitor 1C, or p57, also affects corticogenesis. It has been shown the p57 induces cells to exit from ... The Cyclin-Dependent Kinase Inhibitor p57(Kip2) Regulates Cell Cycle Exit, Differentiation, and Migration of Embryonic Cerebral ... p57 is able to induce neuronal progenitor cells to start differentiating into highly specialized neurons in the cortex. However ... Appropriate functioning and development of the subplate is highly dependent upon organization and connectivity. Disruptions ...

https://en.wikipedia.org/wiki/Development_of_the_cerebral_cortex

"P21-activated kinase 4 regulates the cyclin-dependent kinase inhibitor p57(kip2) in human breast cancer". Anatomical Record. ... "Small-molecule p21-activated kinase inhibitor PF-3758309 is a potent inhibitor of oncogenic signaling and tumor growth". ... "Discovery and the structural basis of a novel p21-activated kinase 4 inhibitor". Cancer Letters. 349 (1): 45-50. doi:10.1016/j. ... a novel and potent p21-activated kinase 4 inhibitor, suppresses proliferation and invasion in human gastric cancer cells". ...

https://en.wikipedia.org/wiki/PAK4

"Cyclin D- and E-dependent kinases and the p57(KIP2) inhibitor: cooperative interactions in vivo". Molecular and Cellular ... Cyclins function as regulators of cyclin-dependent kinases. Different cyclins exhibit distinct expression and degradation ... are specific inhibitors of the cyclin D-dependent kinases CDK4 and CDK6". Molecular and Cellular Biology. 15 (5): 2672-81. doi: ... Meyerson M, Harlow E (Mar 1994). "Identification of G1 kinase activity for cdk6, a novel cyclin D partner". Molecular and ...

https://en.wikipedia.org/wiki/Cyclin_D2

"Cyclin D- and E-dependent kinases and the p57(KIP2) inhibitor: cooperative interactions in vivo". Mol. Cell. Biol. 19 (1): 353- ... Cyclin-dependent kinase 4, Cyclin-dependent kinase 6, EIF3K, and Retinoic acid receptor alpha. Cyclin Cyclin D GRCh38: Ensembl ... Fink JR, LeBien TW (2001). "Novel expression of cyclin-dependent kinase inhibitors in human B-cell precursors". Exp. Hematol. ... Cyclins function as regulators of CDK kinases. Different cyclins exhibit distinct expression and degradation patterns which ...

https://en.wikipedia.org/wiki/Cyclin_D3

... also known as cyclin-dependent kinase inhibitor 1 or CDK-interacting protein 1, is a cyclin-dependent kinase inhibitor (CKI) ... which is homologous to the other CIP/KIP CDK inhibitors p27 and p57. Specifically it contains a Cy1 motif in the N-terminal ... "Mechanism of inhibition of proliferating cell nuclear antigen-dependent DNA synthesis by the cyclin-dependent kinase inhibitor ... "Entrez Gene: CDKN1A cyclin-dependent kinase inhibitor 1A (p21, Cip1)". Gartel AL, Radhakrishnan SK (May 2005). "Lost in ...

https://en.wikipedia.org/wiki/P21

... an anorectic BRM P57, a Formula One racing car Cyclin-dependent kinase inhibitor 1C Papyrus 57, a biblical manuscript P57, a ... P57), a submarine of the Royal Navy INS Sunayna (P57), a patrol vessel of the Indian Navy P57 Kasos, a HSY-55-class gunboat of ... P57 may refer to: Partenavia P.57 Fachiro, an Italian civil utility aircraft Percival P.57 Sea Prince, a British anti-submarine ...

https://en.wikipedia.org/wiki/P57

In addition to p53 and Rb, cyclin dependent kinase inhibitors (CKIs), such as p21, p27, and p57, are also important for ... Immunoprecipitation kinase assays revealed that cyclin C has Rb kinase activity. Furthermore, unlike cyclins D and E, cyclin ... co-immunoprecipitation assays revealed that cyclin-dependent kinase 3 (cdk3) promotes G0 exit by forming a complex with cyclin ... Under normal conditions, the yeast cyclin-dependent kinase complex, Pho80-Pho85, inactivates the Pho4 transcription factor ...

https://en.wikipedia.org/wiki/G0_phase

de Nooij JC; Graber KH; Hariharan IK (2001). "Expression of cyclin-dependent kinase inhibitor Dacapo is regulated by cyclin E ... activity involves Ago/Fbw7-mediated proteolytic degradation of cyclin E and direct inhibition by factors such as Dacapo and p57 ... Entry into endocycles involves modulation of mitotic and S-phase cyclin-dependent kinase (CDK) activity. Inhibition of M-phase ... "A Dominant Negative Mutant of Cyclin-Dependent Kinase A Reduces Endoreduplication but Not Cell Size or Gene Expression in Maize ...

https://en.wikipedia.org/wiki/Endoreduplication

... has been shown to interact with: CDK9 CREB-binding protein Cyclin A1 Cyclin-dependent kinase inhibitor 1C EP300 PARP1 ... "The cell cycle-regulated B-Myb transcription factor overcomes cyclin-dependent kinase inhibitory activity of p57(KIP2) by ... The encoded protein is phosphorylated by cyclin A/cyclin-dependent kinase 2 during the S-phase of the cell cycle and possesses ... April 2001). "Cyclin A1 directly interacts with B-myb and cyclin A1/cdk2 phosphorylate B-myb at functionally important serine ...

https://en.wikipedia.org/wiki/MYBL2

"A current and comprehensive review of cyclin-dependent kinase inhibitors for the treatment of metastatic breast cancer". ... The cip/kip family includes the genes p21, p27 and p57. They halt the cell cycle in G1 phase by binding to and inactivating ... Two key classes of regulatory molecules, cyclins and cyclin-dependent kinases (CDKs), determine a cell's progress through the ... cyclin A, DNA polymerase, thymidine kinase, etc. Cyclin E thus produced binds to CDK2, forming the cyclin E-CDK2 complex, which ...

https://en.wikipedia.org/wiki/Cell_cycle

... cyclin-dependent kinase inhibitor p27 MeSH D12.776.624.776.355.700 - cyclin-dependent kinase inhibitor p57 See List of MeSH ... cyclin-dependent kinase inhibitor p15 MeSH D12.776.624.776.355.200 - cyclin-dependent kinase inhibitor p16 MeSH D12.776.624.776 ... cyclin-dependent kinase inhibitor p18 MeSH D12.776.624.776.355.400 - cyclin-dependent kinase inhibitor p19 MeSH D12.776.624.776 ... cyclin-dependent kinase 5 MeSH D12.776.167.200.067.900 - cyclin-dependent kinase 9 MeSH D12.776.167.200.580.500 - cdc2 protein ...

https://en.wikipedia.org/wiki/List_of_MeSH_codes_(D12.776)

Cyclin-dependent kinase 4, Cyclin-dependent kinase inhibitor 1C, EP300, HDAC1, ID1, ID2, MDFI, MOS, Retinoblastoma protein, ... "Stabilization of MyoD by direct binding to p57(Kip2)". J. Biol. Chem. 275 (25): 18767-76. doi:10.1074/jbc.M907412199. PMID ... MyoD is inhibited by cyclin dependent kinases (CDKs). CDKs are in turn inhibited by p21. Thus MyoD enhances its own activity in ... Both MyoD and pRb are necessary for the repression of cyclin D1, but rather than acting directly on cyclin D1, they act on Fra- ...

https://en.wikipedia.org/wiki/MyoD

cyclin-dependent kinase inhibitor 1C (p57, Kip2). *cyclin-dependent kinase inhibitor p57 ... p57(Kip2)) analysis in Beckwith-Wiedemann syndrome (BWS) patients: Genotype-phenotype correlations, novel mutations, and ... cyclin-dependent kinase inhibitor 1C. * ... CYCLIN-DEPENDENT KINASE INHIBITOR 1C. Gene and Variant ...

https://medlineplus.gov/genetics/gene/cdkn1c/

Cyclin D- and E-dependent kinases and the p57(KIP2) inhibitor: cooperative interactions in vivo. Molecular and cellular biology ... Let-7a functions as a tumor suppressor in Ewings sarcoma cell lines partly by targeting cyclin-dependent kinase 6. DNA and ... CCND2 gene encoded a protein termed G1/S-specific cyclin-D2, which belongs to the highly conserved cyclin family. CCND2 forms a ... Another down-regulated gene, CCND2 (cyclin D2) was picked out. CCND2 is one member of the cyclins that participate in promoting ...

https://www.oncotarget.com/article/14394/text/

Cyclin-dependent kinase inhibitor 1C (CDKN1C) gene, which encodes the cell cycle inhibitor p57KIP2, has been suggested to be ... and cyclin-dependent kinase 9 (CDK9) [15]. Overall, the remodeling in skeletal muscle and heart is perfectly the same as the ... S. Qin, A. Li, M. Yi, S. Yu, M. Zhang, and K. Wu, "Recent advances on anti-angiogenesis receptor tyrosine kinase inhibitors in ... Z. Nahlé, M. Hsieh, T. Pietka et al., "CD36-dependent regulation of muscle FoxO1 and PDK4 in the PPARδ/β-mediated adaptation to ...

https://www.hindawi.com/journals/ppar/2020/3608315/

... directly targeted cell growth-suppressive cyclin-dependent kinase inhibitors p27 and p57 mRNAs, and reduce their protein levels ... The prognostic value and overexpression of cyclin A is correlated with gene amplification of both cyclin A and cyclin E in ... belongs to the highly conserved cyclin family. The gene is expressed in all tissues and binds/activates CDC2 kinases, and thus ... The importance of a gene is often dependent on how well it associates with other genes in a network. Studies suggest that more ...

https://aacrjournals.org/cancerres/article/69/24/9490/552818/Gene-Networks-and-microRNAs-Implicated-in

Cyclin Dependent Kinase Inhibitor 1C Cyclin Dependent Kinase Inhibitor p57 Cyclin Kinase Inhibitor Protein 2 Cyclin-Dependent ... Cyclin Dependent Kinase Inhibitor 1C. Cyclin Dependent Kinase Inhibitor p57. Cyclin Kinase Inhibitor Protein 2. Cyclin- ... Cyclin-Dependent Kinase Inhibitor p57 - Preferred Concept UI. M0245969. Scope note. A potent inhibitor of CYCLIN-DEPENDENT ... Protein Kinase Inhibitors. Public MeSH Note:. 2006; CYCLIN-DEPENDENT KINASE INHIBITOR P57 was indexed under NUCLEAR PROTEINS ...

https://decs.bvsalud.org/en/ths/resource/?id=50933

Cyclin-dependent kinase inhibitors (CDKIs) are proteins that bind to and inhibit the activity of CDKs. Two major classes of CDK ... The p21 family (p21, p27, p28 and p57) can bind to broad range of CDK-cyclin complexes and inhibit their activities. CDKIs are ... Cyclin-dependent kinase 4 inhibitor A, CDK4I, p16-INK4, p16-INK4a, p16INK4A, CDKN-2A, CDKN2, Multiple tumor suppressor 1, MTS1 ... Lyophilized Cyclin-dependent kinase although stable at room temperature for 3 weeks, should be stored desiccated below -18°C. ...

https://www.prospecbio.com/cdkn2a_human

The cyclin-dependent kinase inhibitors p57 and p27 regulate neuronal migration in the developing mouse neocortex.. J Biol Chem. ... Phosphorylation of Xenopus MAP kinase kinase by MAP kinase kinase kinase and MAP kinase. J. Biol. Chem. 268, 3277-3281. (1993) ... A novel kinase cascade mediated by mitogen-activated protein kinase kinase 6 and MKK3.. J. Biol. Chem. 13675-13679. (1996). ... Interaction of MAP kinase with MAP kinase kinase : Its possible role in the control of nucleocytoplasmic transport of MAP ...

https://molbio.f.u-tokyo.ac.jp/japanese/publications.html

cyclin-dependent kinase inhibitor 1C (P57). 0.070. H2-Ab1. histocompatibility 2, class II antigen A, beta 1. 0.062. ...

http://imp.princeton.edu/predictions/process_ortho/fly-context-global/8055/?gene=139479

CDKN1C (cyclin-dependent kinase inhibitor 1C (p57,...)) LOVD v.3.0 Build 28 [ Current LOVD status ]. Register as submitter , ...

https://databases.lovd.nl/shared/genes/CDKN1C

cyclin-dependent kinase inhibitor 1C (p57, Kip2) decreases with age. Molecular. ovary. Human. CDKN1C. 69.3% Decrease Gene ... adenylate kinase 3-like 2; adenylate kinase 3-like 1 increases with age. Molecular. ovary. Human. AK4P3. 54.0% Increase Gene ...

http://beta.ageing-map.org/bibliography/entry/2714/

A cyclin-dependent kinase (CDK) inhibitor, p57Kip2, is an important molecule involved in bone development; p57Kip2-deficient ( ... Inibidor de Quinase Dependente de Ciclina p57/genética , Inibidor de Quinase Dependente de Ciclina p57/metabolismo , ... and protein kinase RNA-like ER kinase (PERK) branches of UPR in LNCaP human prostate cancer cells. Also, similar results were ... Primary p57-/- osteoblasts exhibited higher proliferation rates with Cdk activation than p57+/+ cells. A lower level of nodule ...

https://pesquisa.bvsalud.org/bolivia/?lang=pt&q=mh:Receptores+de+Calcitriol/gen%C3%A9tica

... and the c-Jun NH2-terminal kinase (JNK) signaling pathway, as well as their roles in OS of melanoma cells were identified. ... Through loss and gain of function experiments, the interactions between miR-517a, the cyclin dependent kinase inhibitor 1C ( ... p57KIP2) belongs to the cyclin-dependent kinase (CDK) inhibitors of the Cip/Kip family, which participate in several cellular ... the cyclin dependent kinase inhibitor 1C (CDKN1C) and the c-Jun NH2-terminal kinase (JNK) signaling pathway, as well as their ...

https://cancerci.biomedcentral.com/articles/10.1186/s12935-019-1064-y

Cyclin-Dependent Kinases 28% * Cyclin-Dependent Kinase Inhibitor p15 21% 27 Scopus citations ... A potential role for p15(Ink4b) and p57(Kip2) in liver development. Awad, M. M., Sanders, J. A. & Gruppuso, P. A., Oct 20 2000 ... Antibody directs properdin-dependent activation of the complement alternative pathway in a mouse model of abdominal aortic ... A phase II trial of neoadjuvant MK-2206, an AKT inhibitor, with anastrozole in clinical stage II or III PIK3CA-mutant ER- ...

https://profiles.wustl.edu/en/organisations/division-of-general-surgery/publications/?type=%2Fdk%2Fatira%2Fpure%2Fresearchoutput%2Fresearchoutputtypes%2Fcontributiontojournal%2Farticle&ordering=type&descending=false&page=4

... proliferation associated with activation of numerous neuronal genes and genes encoding cyclin-dependent kinase inhibitors (p16/ ... p19 and p57). Furthermore, the chromodomain- and SUMO E3 ligase-dependent Cbx4 activities differentially regulate proliferation ... identity and proliferative activity in KCs via repression of the selected nonepidermal lineage and cell cycle inhibitor genes. ...

https://bradscholars.brad.ac.uk/handle/10454/10161

... and the cyclin-dependent kinase (CDK) inhibitors p27 and p57 was observed[38]. MiR-21 is a well described oncomir; however, DIM ... The indole-based protein kinase inhibitors sunitinib (approved for the treatment of metastatic renal cell carcinoma) and ... protein kinase inhibitors), endocrine therapy, and immunotherapy[1-3]. However, efficient cancer treatment with ... Compound 10 led to G2 cell cycle arrest by upregulation of cyclin B1 expression and phosphor-cdc-2 in the breast cancer cells. ...

https://cdrjournal.com/article/view/3692

Mechanisms of cyclin-dependent kinase regulation: structures of Cdks, their cyclin activators, and Cip and INK4 inhibitors. J ... Oya, M. and Schulz, W.A. (2000) Decreased expression of p57(KIP2) mRNA in human bladder cancer. Br. J. Cancer 83, 626-631. 26. ... Development of cyclin-dependent kinase modulators as novel therapeutic approaches for hematological malignancies. Leukemia 2001 ... Preclinical and clinical development of cyclin-dependent kinase modulators. J Natl Cancer Inst 2000;92: 376-387.. 35. Sherr CJ ...

https://ajpsonline.com/AbstractView.aspx?PID=2021-11-2-14

p57 KIP2 Protein use Cyclin-Dependent Kinase Inhibitor p57 p57KIP2 Protein use Cyclin-Dependent Kinase Inhibitor p57 ... p21 Cell Cycle Regulator use Cyclin-Dependent Kinase Inhibitor p21 p21 Cyclin Kinase Inhibitor use Cyclin-Dependent Kinase ... p27 CDK Inhibitor use Cyclin-Dependent Kinase Inhibitor p27 p27 Kip1 Protein use Cyclin-Dependent Kinase Inhibitor p27 ... p27, CDK Inhibitor use Cyclin-Dependent Kinase Inhibitor p27 p27Kip1 Protein use Cyclin-Dependent Kinase Inhibitor p27 ...

https://decs.bvs.br/I/DeCS2016_Alfab-P.htm

CDKN1C encodes a cyclin-dependent kinase inhibitor belonging to the CIP family of cell-cycle regulators. Overexpression of ... A human p57(KIP2) transgene is not activated by passage through the maternal mouse germline. Hum. Mol. Genet. 1999. 8:2211-2219 ... Thus, overexpression of IGF2 in transgenic mice causes overgrowth, macroglossia, and organomegaly in a dose-dependent fashion ( ...

https://www.jci.org/articles/view/9340

https://decs2020.bvsalud.org/I/DeCS2019_Alfab-P.htm

https://decs2019.bvsalud.org/I/DeCS2018_Alfab-P.htm

https://decs2018.bvsalud.org/I/DeCS2017_Alfab-P.htm

https://decs2017.bvsalud.org/I/DeCS2017_Alfab-P.htm

Previous studies have confirmed that miR-221 also inhibits the expressions of the PTEN and cyclin-dependent kinase inhibitor ... Sun, K., Wang, W., Zeng, J.-j., Wu, C.-t., Lei, S.-t., and Li, G.-x. (2011). MicroRNA-221 Inhibits CDKN1C/p57 Expression in ... The results showed that FAM green fluorescence was increased in Caco2 and HCT116 cells in a dose-dependent manner (Figure 2E), ... The sediment contained the compound exosomes loaded with miR-221 inhibitor (AMO-Exos), and stored at −80°C for standby use. ...

https://www.frontiersin.org/articles/10.3389/fmolb.2021.743013/full

... however this protein is known to interact with DNA-dependent protein kinase and may play a role in kinase-phosphatase ... The cells were lysed in modified RIPA buffer (25mM Tris-HCl pH7.6, 150mM NaCl, 1% NP-40, 1mM EDTA, 1xProteinase inhibitor ... IRE1 alpha dependent apoptotic-signaling pathway. Despite in depth characterization of the role of IRE1 alpha (inositol- ...

https://www.novusbio.com/products/cib1-lysate_nbl1-09204

Munirah, I., Immortalization of cells derived from domestic dogs through expressing mutant cyclin-dependent kinase 4, cyclin D1 ... Ehata, S., Ki26894, a novel transforming growth factor-beta type I receptor kinase inhibitor, inhibits in vitro invasion and in ... Takahashi, S., Loss of p57 KIP2 expression confers resistance to contact inhibition in human androgenetic trophoblast stem ... Bovine and porcine fibroblasts can be immortalized with intact karyotype by the expression of mutant cyclin dependent kinase 4 ...

https://dnaconda.riken.jp/search/RDB_clone/RDB04/RDB04394.html

Casein Kinase-2. *Creatin Kinases. *Cyclin. *Cyclin-Dependent Kinase. *Cyclophilin. *Deaminase. *Decarboxylase ... BWCR; BWS; KIP2; WBS; p57;. 100ul. 200ul. $220. Add to Cart A2010. Rabbit. BAG6. G3; BAT3; BAG-6; D6S52E;. 100ul. 200ul. $220. ...

https://neobiolab.com/monoclonal-antibodies/8.html

CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... Finally, the Akt protein kinase promotes cell survival through two pathways. Akt phosphorylates and inhibits Bad (a Bcl-2 ... Caspases are proteins that are highly conserved, cysteine-dependent aspartate-specific proteases. There are two types of ... Cyclin. *A (A1, A2). *B (B1, B2, B3). *D (D1, D2, D3) ... Using these inhibitors it was discovered that cells can die ...

https://mdwiki.org/wiki/Proapoptotic

Open in another window Amount 4 Substance 7ae inhibited LPS-induced IL-6 and TNF- discharge within a dose-dependent way in MPMs ... Additionally, PRL treatment may defend (straight or indirectly) against induction of FoxO1, p27, p57, and menin and/or lack of ... Further analysis demonstrated a hydrophilic group at R2 contributed greatly towards the DDR1 kinase inhibition also. When the 1 ... A and B cyclins below stress, simply because suggested simply by our studies of the consequences of DEX and glucose deprivation ...

http://www.eotp.org/2021/11/21/%EF%BB%BF115766-janssen-merck-co/

Through loss and gain of function experiments, the interactions between miR-517a, the cyclin dependent kinase inhibitor 1C (CDKN1C) and the c-Jun NH2-terminal kinase (JNK) signaling pathway, as well as their roles in OS of melanoma cells were identified. (biomedcentral.com)
revealed that miR-221 affects the occurrence and progression of colorectal carcinoma (CRC) by targeting cyclin dependent kinase inhibitor 1C (CDKN1C), a key modulator of cell cycle progression [ 15 ]. (biomedcentral.com)
CDKN1C (p57 KIP2 ) belongs to the cyclin-dependent kinase (CDK) inhibitors of the Cip/Kip family, which participate in several cellular processes in human cancers [ 16 ]. (biomedcentral.com)
CDKN1C is reported to be a cell-cycle kinase inhibitor and has the potential to inhibit the c-Jun N-terminal kinase (JNK) signaling pathway in chronic inflammatory diseases [ 18 ]. (biomedcentral.com)

The current treatments of cancer comprise of surgery, radiation therapy, chemotherapy with classical cytotoxic drugs and/or targeted drugs (e.g., protein kinase inhibitors), endocrine therapy, and immunotherapy [ 1 - 3 ] . (cdrjournal.com)
The indole-based protein kinase inhibitors sunitinib (approved for the treatment of metastatic renal cell carcinoma) and enzastaurin were developed based on the natural lead indole derivative staurosporin [ 8 - 10 ] . (cdrjournal.com)
Cyclin: a protein specified by maternal mRNA in sea urchin eggs that is destroyed at each cleavage division. (ajpsonline.com)
however this protein is known to interact with DNA-dependent protein kinase and may play a role in kinase-phosphatase regulation of DNA end joining. (novusbio.com)

Cyclin-dependent kinase inhibitors (CDKIs) are proteins that bind to and inhibit the activity of CDKs. (prospecbio.com)
The p21 family (p21, p27, p28 and p57) can bind to broad range of CDK-cyclin complexes and inhibit their activities. (prospecbio.com)

Furthermore, the chromodomain- and SUMO E3 ligase-dependent Cbx4 activities differentially regulate proliferation, differentiation, and expression of nonepidermal genes in KCs. (brad.ac.uk)

We also found that cyclin D2 (CCND2) was a novel target gene of miR-124, and was directly involved in miR-124-mediated suppressive effects on cell growth. (oncotarget.com)

The Cell Cycle, Cyclins, Checkpoints and Cancer. (ajpsonline.com)
2001) Reduced expression and impaired kinase activity of a Chk2 mutant identified in human lung cancer. (ajpsonline.com)

These data demonstrate that Cbx4 plays a crucial role in the p63-regulated program of epidermal differentiation, maintaining the epithelial identity and proliferative activity in KCs via repression of the selected nonepidermal lineage and cell cycle inhibitor genes. (brad.ac.uk)
When 1-(4-methyl)piperazinylmethyl moiety was transferred at R5 placement, the resulting compound 7s abolished the kinase activity. (eotp.org)

In humans, aberrant expression of p57 is associated with various NEOPLASMS as well as with BECKWITH-WIEDEMANN SYNDROME. (bvsalud.org)

Indoles are also prominent dietary compounds, and indole alkaloid derivatives of Brassica species such as indole glucosinolates, indole-3-carbinol (I3C), and 3,3'-diindolylmethane (DIM) display distinct anticancer activities based on apoptosis induction as well as suppression of phosphatidyl-inositol-3-kinase(PI3K)/Akt and nuclear factor κB (NF-κB) signaling [Figure 1] [ 11 - 13 ] . (cdrjournal.com)

Inhibitory Actions of Substances 7aC7j against DDR1, DRR2, Bcl-Abl, and c-Kita Open up in another window Open up in another screen aDDR1 and AZD7762 DDR2 tests had been performed using LANCE ULTRA kinase assay based on the producers instructions. (eotp.org)

The cyclin-dependent kinase inhibitor p57(KIP2) is thought to be a potential tumor suppressor gene (TSG). (nih.gov)
We found that the expression of p57(KIP2) gene is absent in various hematological cell lines. (nih.gov)
Exposing cell lines to the DNA demethylating agent 5-aza-2'-deoxycytidine restored p57(KIP2) gene expression. (nih.gov)
Bisulfite sequencing analysis of its promoter region showed that p57(KIP2) DNA was completely methylated in cell lines that did not express the p57(KIP2) gene. (nih.gov)
Thus, DNA methylation of its promoter might lead to inactivation of the p57(KIP2) gene. (nih.gov)
Methylation-specific polymerase chain reaction analysis found frequent DNA methylation of the p57(KIP2) gene in primary diffuse large B-cell lymphoma (54.9%) and in follicular lymphoma (44.0%), but methylation was infrequent in myelodysplastic syndrome and adult T-cell leukemia (3.0% and 2.0%, respectively). (nih.gov)
These findings directly indicate that the profile of the p57(KIP2) gene corresponds to that of a TSG. (nih.gov)
Methylation of p16(INK4A) and p57(KIP2) are involved in the development and progression of gastric MALT lymphomas. (nih.gov)
CDK activity is modulated by the CDKIs p27 kip1 , p57 kip2 , p16 ink4A , p15 ink4B , p18 ink4C , and p19 ink4D . (medscape.com)
3. Expression of p57(KIP2) in hepatocellular carcinoma: relationship between tumor differentiation and patient survival. (nih.gov)
6. Contrasting roles of p57(KIP2) and p21(WAF1/CIP1/SDI1) in transplanted human and bovine adrenocortical cells. (nih.gov)
7. Expression of p21(Wafl/Cip1), p57(Kip2) and HER2/neu in patients with gallbladder cancer. (nih.gov)
p57(kip2), is involved in the cell cycle progression of vascular smooth muscle cells. (nih.gov)
11. Cyclic changes in the expression of p57(kip2) in human endometrium and its regulation by steroid hormones in endometrial stromal cells in vitro. (nih.gov)
13. Significance of p57(Kip2) down-regulation in oncogenesis of bladder carcinoma: an immunohistochemical study. (nih.gov)
14. [Relationship between expression of p57(kip2), cyclin E protein, PCNA, and clinicopathological factors in human pancreatic cancer]. (nih.gov)
15. p57(Kip2) and cancer: time for a critical appraisal. (nih.gov)
16. Downregulation of the KIP family members p27(KIP1) and p57(KIP2) by SKP2 and the role of methylation in p57(KIP2) inactivation in nonsmall cell lung cancer. (nih.gov)
We also found that the cyclin-dependent kinase inhibitor Kip2/p57 gene is a specific target of p73 regulation during mitotic exit and re-entry into G1. (elsevier.com)
Both knock-out of p73 gene expression by siRNAs and abrogation of p73-dependent transcription by the p73DD mutant abrogate Kip2/p57 increase at the M-to-G 1 transition. (elsevier.com)
Moreover, similar abnormalities (e.g. delay in late mitotic stages with the accumulation of aberrant ana-telophase figures, and abnormalities in the following interphase) are observed in cultures in which the expression of Kip2/p57 is abrogated by siRNAs. (elsevier.com)
These results identify a novel p73-Kip2/p57 pathway that coordinates mitotic exit and transition to G 1 . (elsevier.com)

Cell Cycle Regulation The cell cycle is regulated by cyclins, cyclin-dependent kinases (CDKs), and cyclin-dependent kinase inhibitors (CDKIs) and is divided into 4 distinct phases (G1, S, G2, and M). G0 represents exit from the cell cycle. (slideserve.com)
The cell cycle is driven by CDKs, which are positively and negatively regulated by cyclins and CDKIs, respectively. (slideserve.com)
Cyclins, cyclin-dependent kinases (CDKs) and CDK inhibitors (CDKIs) regulate cell-cycle progression. (medscape.com)
The four sequential stages (G1, S, G2, and M) of cell cycle progression are positively regulated by complexes of cyclin-dependent kinases (CDKs) and associated cyclins, which are negatively regulated by cyclin-dependent kinase inhibitors (CKIs). (researchsquare.com)
Transitions between cell-cycle stages are mediated by cyclin-dependent kinases (Cdks) and their modulators. (perlierusa.com)
Cdks could be managed by Cdk inhibitors (CKIs) that bind to Cdks (12,13). (perlierusa.com)
The cyclin-dependent kinase (CDK) inhibitors p21 and p16 inhibit the activity of CDKs, such as CDK4. (medscape.com)

The encoded protein is a tight-binding, strong inhibitor of several G1 cyclin/Cdk complexes and a negative regulator of cell proliferation. (nih.gov)
Cyclin-dependent kinase 2 , also known as cell division protein kinase 2 , or Cdk2, is an enzyme that in humans is encoded by the CDK2 gene . (wikipedia.org)
[5] [6] The protein encoded by this gene is a member of the cyclin-dependent kinase family of Ser/Thr protein kinases . (wikipedia.org)
This protein kinase is highly similar to the gene products of S. cerevisiae cdc28 , and S. pombe cdc2, also known as Cdk1 in humans. (wikipedia.org)
This protein associates with and is regulated by the regulatory subunits of the complex including cyclin E or A . Cyclin E binds G1 phase Cdk2, which is required for the transition from G1 to S phase while binding with Cyclin A is required to progress through the S phase. (wikipedia.org)
Cdk2 becomes active when a cyclin protein (either A or E) binds at the active site located between the N and C lobes of the kinase. (wikipedia.org)
The p16INK4A protein is a cell-cycle inhibitor that acts by inhibiting activated cyclin D:CDK4/6 complexes, which play a crucial role in the control of the cell cycle by phosphorylating Rb protein. (medscape.com)
Furthermore, the link between some tumor suppressors and survival genes, such as the link between PTEN and the survival effector, AKT (also known as protein kinase B or PKB), may indicate therapeutic means of targeting metastasis, tumor growth, and cancer survival. (hindawi.com)

The INK4 gene family, including p15, p16, p18, and p19, bind to CDK4 and CDK6 and inhibit their kinase activities by interfering with their association with D-type cyclins. (researchsquare.com)

Potent tight-binding inhibitor of several G1 cyclin/CDK complexes (cyclin E-CDK2, cyclin D2-CDK4, and cyclin A-CDK2) and, to lesser extent, of the mitotic cyclin B-CDC2. (nih.gov)

2. Expression of cell cycle inhibitor p27Kip1 and its inactivator Jab1 in melanocytic lesions. (nih.gov)
4. Persistent and heterogenous expression of the cyclin-dependent kinase inhibitor, p27KIP1, in rat hearts during development. (nih.gov)

An INK4 cyclin-dependent kinase inhibitor containing four ANKYRIN-LIKE REPEATS. (bvsalud.org)

Expression of tumor-promoting factors by senescent cells is mediated, at least in part, by senescence-associated cyclin-dependent kinase inhibitors such as p21 Waf1/Cip1/Sdi1 . (aacrjournals.org)

Most human malignancies are driven by chromosomal translocations or other genetic alterations that directly affect the function of critical cell cycle proteins such as cyclins as well as tumor suppressors, e.g., p53. (springer.com)
Another important class of tumor suppressor genes involved in cell cycle control and in the generation of human cancers is the cyclin-dependent kinase (CDK) inhibitors. (medscape.com)

Moreover, the HSC abnormalities of p57-deficient mice were corrected by knocking in the p27 gene at the p57 locus. (elsevier.com)

1. Different expression patterns of p27 and p57 proteins in benign and malignant melanocytic neoplasms and in cultured human melanocytes. (nih.gov)
It is a catalytic subunit of the cyclin-dependent kinase complex, whose activity is restricted to the G1-S phase of the cell cycle , where cells make proteins necessary for mitosis and replicate their DNA. (wikipedia.org)

In humans, aberrant expression of p57 is associated with various NEOPLASMS as well as with BECKWITH-WIEDEMANN SYNDROME . (nih.gov)
Aberrant gene expression, such as cyclin-dependent kinases CDK6 and cyclin-dependent kinase inhibitor p27, was found in the prenatal D4-treated mice. (researchsquare.com)

Cdk2 (blue) and its binding partner, cyclin A (red). (wikipedia.org)
Due to the location of the active site, partner cyclins interact with both lobes of Cdk2. (wikipedia.org)
Cdk2 contains an important alpha helix located in the C lobe of the kinase, called the C-helix or the PSTAIRE-helix. (wikipedia.org)
It is important to note that throughout this activation process, cyclins binding to Cdk2 do not undergo any conformational change. (wikipedia.org)

CD36 and TAM (Tyrosine Kinase Mer) receptor, which have been suggested to be PS receptors and associated with phagocytosis, were proposed as the receptors of the signaling pathway mediating TGF production, but this is still controversial1,12. (africagis2009.org)

The significance of this movement is that it brings the side chain of Glu 51, which belongs to a triad of catalytic site residues conserved in all eukaryotic kinases, into the catalytic site. (wikipedia.org)

DNA damage increases TP53 levels through an ATM-dependent pathway. (medscape.com)

The success of the cell division process is dependent on the precise regulation of processes at both cellular and tissue levels. (cloudfront.net)

A potent inhibitor of CYCLIN-DEPENDENT KINASES in G1 PHASE and S PHASE . (nih.gov)
Here we show a severe defect in the self-renewal capacity of p57-deficient HSCs and a reduction of the proportion of the cells in G 0 phase. (elsevier.com)

Members of the Cip/Kip family of cyclin-dependent kinase (CDK) inhibitors (p21, p27, p57) have been implicated in HSC quiescence, but loss of p21 or p27 in mice affects HSC quiescence or functionality only under conditions of stress. (elsevier.com)

Although p57 is the most abundant family member in quiescent HSCs, its role has remained uncharacterized. (elsevier.com)
Our results therefore suggest that, among Cip/Kip family CDK inhibitors, p57 plays a predominant role in the quiescence and maintenance of adult HSCs. (elsevier.com)

Anatomy7

Organisms2

Chemicals and Drugs72

Analytical, Diagnostic and Therapeutic Techniques and Equipment5

Phenomena and Processes29

Disciplines and Occupations1

Information Science3

p57(Kip2) is degraded through the proteasome in osteoblasts stimulated to proliferation by transforming growth factor beta1. (1/288)

Analysis of germline CDKN1C (p57KIP2) mutations in familial and sporadic Beckwith-Wiedemann syndrome (BWS) provides a novel genotype-phenotype correlation. (2/288)

CDKN1C expression in Beckwith-Wiedemann syndrome patients with allele imbalance. (3/288)

TGF-beta1-mediated hypertrophy involves inhibiting pRB phosphorylation by blocking activation of cyclin E kinase. (4/288)

Spatial and temporal expression of p57(KIP2) during murine lens development. (5/288)

p57KIP2 expression and loss of heterozygosity during immortal conversion of cultured human mammary epithelial cells. (6/288)

A human p57(KIP2) transgene is not activated by passage through the maternal mouse germline. (7/288)

Mechanism for inactivation of the KIP family cyclin-dependent kinase inhibitor genes in gastric cancer cells. (8/288)

Cyclin-Dependent Kinase Inhibitor p27

Cyclin-Dependent Kinase Inhibitor p21

Cyclin-Dependent Kinases

Cyclins

Cell Cycle Proteins

Cyclin-Dependent Kinase Inhibitor p16

Cell Cycle

Tumor Suppressor Proteins

Microtubule-Associated Proteins

Cyclin-Dependent Kinase 2

Cyclin D1

Cyclin A

Cyclin E

Cell Proliferation

Cyclin-Dependent Kinase 4

CDC2-CDC28 Kinases

Apoptosis

Cyclin-Dependent Kinase Inhibitor p57

Cell Line, Tumor

Protein Kinase Inhibitors

Protein-Serine-Threonine Kinases

G1 Phase

Cyclin-Dependent Kinase 5

Cyclin B

Cyclin D

CDC2 Protein Kinase

Cyclin-Dependent Kinase Inhibitor Proteins

Cyclin C

Phosphorylation

Cyclin D3

Retinoblastoma Protein

Cyclin-Dependent Kinase 6

Cell Division

Enzyme Inhibitors

S Phase

Cyclin B1

Cyclin-Dependent Kinase Inhibitor p18

Tumor Suppressor Protein p53

Proto-Oncogene Proteins

Tumor Cells, Cultured

Signal Transduction

Cyclin D2

Cells, Cultured

Phosphatidylinositol 3-Kinases

Blotting, Western

E2F1 Transcription Factor

Cyclin A1

Protein Kinases

Purines

Transfection

Cell Line

Mitosis

Cyclin G

G2 Phase

Transcription Factor DP1

Mutation

Proliferating Cell Nuclear Antigen

Cyclin-Dependent Kinase Inhibitor p15

DNA-Binding Proteins

Cyclin G1

MAP Kinase Signaling System

Cyclin A2

E2F Transcription Factors

RNA, Messenger

Molecular Sequence Data

Carrier Proteins

Nuclear Proteins

Antineoplastic Agents

Transcription Factors

Base Sequence

Protein-Tyrosine Kinases

Calcium-Calmodulin-Dependent Protein Kinases

Immunohistochemistry

Cyclin-Dependent Kinase Inhibitor p19

S-Phase Kinase-Associated Proteins

src-Family Kinases

Enzyme Activation

Down-Regulation

Gene Expression Regulation

Protein Binding