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.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.Cyclin-Dependent Kinases: 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.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 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.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.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.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.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.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.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.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.Cyclin E: A 50-kDa protein that complexes with CYCLIN-DEPENDENT KINASE 2 in the late G1 phase of the cell cycle.Cell Proliferation: All of the processes involved in increasing CELL NUMBER including CELL DIVISION.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.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.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 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.Cell Line, Tumor: A cell line derived from cultured tumor cells.Protein Kinase Inhibitors: Agents that inhibit PROTEIN KINASES.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.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.Cyclin-Dependent Kinase 5: 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.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.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.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.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.Cyclin C: 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.Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.Cyclin D3: A broadly expressed type D cyclin. Experiments using KNOCKOUT MICE suggest a role for cyclin D3 in LYMPHOCYTE development.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.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.Cell Division: The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.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.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.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.Cyclin-Dependent Kinase Inhibitor p18: 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.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.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.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.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.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.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.Phosphatidylinositol 3-Kinases: 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.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.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.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.Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein.Purines: 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.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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.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.Cyclin G: A cyclin subtype that is found associated with CYCLIN-DEPENDENT KINASE 5; cyclin G associated kinase, and PROTEIN PHOSPHATASE 2.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.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.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.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.Cyclin-Dependent Kinase Inhibitor p15: An INK4 cyclin-dependent kinase inhibitor containing four ANKYRIN-LIKE REPEATS. INK4B is often inactivated by deletions, mutations, or hypermethylation in HEMATOLOGIC NEOPLASMS.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 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.MAP Kinase Signaling System: 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.Cyclin A2: A widely-expressed cyclin A subtype that functions during the G1/S and G2/M transitions of the CELL CYCLE.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.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.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.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.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.Antineoplastic Agents: Substances that inhibit or prevent the proliferation of NEOPLASMS.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Protein-Tyrosine Kinases: Protein kinases that catalyze the PHOSPHORYLATION of TYROSINE residues in proteins with ATP or other nucleotides as phosphate donors.Calcium-Calmodulin-Dependent Protein Kinases: 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)Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Cyclin-Dependent Kinase Inhibitor p19: An INK4 cyclin-dependent kinase inhibitor containing five ANKYRIN REPEATS. Aberrant expression of this protein has been associated with TESTICULAR CANCER.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.src-Family Kinases: 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.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.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.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.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.Protein Kinase C: 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.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.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.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.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.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.p38 Mitogen-Activated Protein Kinases: 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.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.Mitogen-Activated Protein Kinases: 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).Mitogen-Activated Protein Kinase 1: 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.Mitogen-Activated Protein Kinase Kinases: 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.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.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.Pyrimidines: 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.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.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Cyclic AMP-Dependent Protein Kinases: 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.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.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)Mitogen-Activated Protein Kinase 3: 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.Proto-Oncogene Proteins c-akt: 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.Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.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.Benzamides: BENZOIC ACID amides.Kinetics: The rate dynamics in chemical or physical systems.JNK Mitogen-Activated Protein Kinases: 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.Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.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.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Cyclin B2: 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.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.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Flavonoids: A group of phenyl benzopyrans named for having structures like FLAVONES.Mice, Inbred C57BLChromones

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)

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Shop Beckwith-Wiedemann syndrome chromosomal region 1 candidate gene B protein ELISA Kit, Recombinant Protein and Beckwith-Wiedemann syndrome chromosomal region 1 candidate gene B protein Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
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J:96366 Cerrato F, Sparago A, Di Matteo I, Zou X, Dean W, Sasaki H, Smith P, Genesio R, Bruggemann M, Reik W, Riccio A, The two-domain hypothesis in Beckwith-Wiedemann syndrome: autonomous imprinting of the telomeric domain of the distal chromosome 7 cluster. Hum Mol Genet. 2005 Feb 15;14(4):503-11 ...
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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
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Beckwith-Wiedemann syndrome (BWS) is a well-studied human overgrowth disorder, associated with visceromegaly, exomphalos, and predisposition to Wilms tumor and other pediatric cancers. BWS is a clinical syndrome, not a single disorder. Phenotypic heterogeneity is prominent, and we now appreciate that this reflects an underlying molecular heterogeneity. The syndrome can be caused by various molecular defects, which lead to altered expression of certain imprinted genes on chromosome 11p15. Multiple studies have revealed striking epigenotype-phenotype correlations, in which exomphalos tracks with one type of imprinting defect, affecting the CDKN1C gene, while Wilms tumor predisposition tracks with a different imprinting defect, affecting the IGF2 and H19 genes. Here we review the clinical and molecular features of BWS and summarize the data from these recent investigations. We also review the fascinating association of BWS with twinning, and discuss preliminary studies suggesting an increased ...
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CDKN2AIPNL - CDKN2AIPNL (untagged)-Human CDKN2A interacting protein N-terminal like (CDKN2AIPNL) available for purchase from OriGene - Your Gene Company.
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TY - JOUR. T1 - Molecular diagnosis of Beckwith-Wiedemann Syndrome using quantitative methylation-sensitive polymerase chain reaction. AU - Coffee, Bradford. AU - Muralidharan, Kasinathan. AU - Highsmith, William E.. AU - Lapunzina, Pablo. AU - Warren, Stephen T.. PY - 2006/10/1. Y1 - 2006/10/1. N2 - PURPOSE: Beckwith-Wiedemann Syndrome is caused by defects in imprinted gene expression at 11p15. Currently, quantitative Southern analysis using DNA methylation-sensitive restriction enzymes is used in molecular diagnosis of this syndrome. METHODS: We describe a rapid and highly quantitative test for assessing DNA methylation at 11p15 using sodium bisulfite treatment of genomic DNA coupled with quantitative TaqMan methylation-sensitive polymerase chain reaction. RESULTS: TaqMan MSP can assess DNA methylation at both differentially methylated region (DMR)1 and DMR2 at 11p15. In addition, by using TaqMan MSP we were able to determine the parent of origin of a duplication of 11p15 by quantification of ...
Features include: macroglossia, a large tongue which may cause breathing, feeding or speech difficulties; umbilical hernia or exomphalos; overgrowth, children are bigger than their contemporaries; hemihypertrophy, one side of the body grows more than the other; hypoglycaemia, low blood sugar as babies; characteristic facial appearance and indentations of the ears.
Recombinant human CDKN1B protein, fused to His-tag at N-terminus, was expressed in E. coli and purified by using conventional chromatography. MW: 24.2 kDa.
TABLE-US-00006 TABLE 6 THI + 2 + 4 + 5 + 7 Composite (Meta-THc) OG- OG- OG- OG- OG- 3116 @ 3116 @ 3116 @ 3116 @ 3116 @ 50 100 1 μg/ml 5 μg/ml 25 μg/ml μg/ml μg/ml Abl(H396P)(h) 91 88 73 55 50 Abl(M351T)(h) 100 87 62 50 38 Abl(Q252H)(h) 89 86 58 45 44 Abl(h) 98 85 65 41 49 Abl(m) 99 87 60 47 43 Abl(T315I)(h) 100 91 79 65 52 Abl(Y253F)(h) 93 90 75 54 51 ACK1(h) 122 112 97 102 82 ALK(h) 76 38 17 16 26 ALK4(h) 96 95 85 68 48 Arg(h) 94 91 68 52 42 Arg(m) 100 99 94 73 50 ARK5(h) 100 97 82 64 75 Aurora-A(h) 92 79 40 41 27 Axl(h) 97 99 83 77 60 Blk(m) 95 102 71 49 54 Bmx(h) 91 94 84 77 43 BrSK1(h) 95 90 71 47 51 BrSK2(h) 91 82 77 70 63 BTK(h) 99 97 64 44 28 CaMKI(h) 95 84 46 28 48 CaMKII(r) 97 106 89 69 63 CaMKIIβ(h) 94 99 85 52 34 CaMKIIγ(h) 107 103 94 92 134 CaMKIIδ(h) 103 97 84 83 84 CaMKIV(h) 107 108 95 75 58 CaMKIδ(h) 91 93 92 75 80 CDK1/cyclinB(h) 99 101 91 71 58 CDK2/cyclinA(h) 105 106 92 83 63 CDK2/cyclinE(h) 99 103 75 60 42 CDK3/cyclinE(h) 108 100 96 79 45 CDK5/p25(h) 102 89 84 77 72 ...
Harrison, T.A., Smith Adams, L.B., Moore, P.D., Perna, M.K., Sword, J.D.and Defoe, D. M.. Accelerated turnover of taste bud cells in mice deficient for the cyclin-dependent kinase inhibitor p27Kip1.BMC Neuroscience 2011, 12:34 ...
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The p57(Kip2) cyclin-dependent kinase inhibitor (CDKi) has been implicated in embryogenesis, stem-cell senescence and pathologies, but little is known of its role in cell cycle control. Here, we show that p57(Kip2) is ...
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Beckwith-Wiedemann syndromeDefinitionBeckwith-Wiedemann syndrome (BWS) refers to a disorder of overgrowth. This condition is usually characterized by large body size (macrosomia), large tongue (macroglossia), enlarged internal organs (visceromegaly), the presence of an abdominal wall defect (umbilical hernia or omphalocele ), and low blood sugar in the newborn period (neonatal hypoglycemia). Source for information on Beckwith-Wiedemann Syndrome: Gale Encyclopedia of Genetic Disorders dictionary.
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.
A collection of disease information resources and questions answered by our Genetic and Rare Diseases Information Specialists for Beckwith-Wiedemann syndrome
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ABERDEEN, S.D. - A South Dakota baby born with a tongue the size of an adults is smiling easily after a life-changing surgery. Little Paisley Morrison-Johnson, now 16 months old, was diagnosed with Beckwith-Wiedemann syndrome when she was born.
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The Beckwith-Wiedemann syndrome, originally described by Beckwith in 1963 and Wiedemann in 1964, included congenital anomalies such as macroglossia, exomphalos, postnatal somatic gigantism, severe hypoglycemia, abdominal wall defect, capillary nevus flameus and hemihypertrophy. Macroglossia is the most common manifestation of Beckwith-Wiedemann syndrome, with studies reporting between 82 and 95 percent of the cases. Macroglossia may cause the upper airway obstruction, deglutition difficulty, articulation interference and protrusion of dentoalveloar structures resulting in anterior open bite and a mandibular prognathism. We experienced a 5 month-old male with upper airway obstruction, deglutition difficulty and recurrent upper airway infection due to macroglossia associated with Beckwith-Wiedemann syndrome and significant improvement in respiration, feeding and oral competence at 14 months follow-up after rhomboid resection and primary closure of tongue. ...
We report on an 8-month-old girl with a novel unbalanced chromosomal rearrangement, consisting of a terminal deletion of 4p and a paternal duplication of terminal 11p. Each of these is associated with the well-known clinical phenotypes of Wolf-Hirschhorn syndrome (WHS) and Beckwith-Wiedemann syndrome (BWS), respectively. She presented for clinical evaluation of dysmorphic facial features, developmental delay, atrial septal defect (ASD), and left hydro-nephrosis. High-resolution cytogenetic analysis revealed a normal female karyotype, but subtelomeric fluorescence in situ hybridization (FISH) analysis revealed a der(4)t(4;11) (pter;pter). Both FISH and microarray CGH studies clearly demonstrated that the WHS critical regions 1 and 2 were deleted, and that the BWS imprinted domains (ID) 1 and 2 were duplicated on the der(4). Parental chromosome analysis revealed that the father carried a cryptic balanced t(4;11)(pter;pter). As expected, our patient manifests findings of both WHS (a growth ...
The combination of intrauterine growth restriction, metaphyseal dysplasia, adrenal hypoplasia congenita, and genital anomalies is commonly known by the acronym IMAGe. This rare syndrome has signs and symptoms that affect many parts of the body.. Most affected individuals grow slowly before birth (intrauterine growth restriction) and are small in infancy. They have skeletal abnormalities that often become apparent in early childhood, although these abnormalities are usually mild and can be difficult to recognize on x-rays. The most common bone changes are metaphyseal dysplasia and epiphyseal dysplasia; these are malformations of the ends of long bones in the arms and legs. Some affected individuals also have an abnormal side-to-side curvature of the spine (scoliosis) or thinning of the bones (osteoporosis).. Adrenal hypoplasia congenita is the most severe feature of IMAGe syndrome. The adrenal glands are a pair of small glands on top of each kidney. They produce a variety of hormones that ...
The cortactin oncoprotein is frequently overexpressed in head and neck squamous cell carcinoma (HNSCC), often due to amplification of the encoding gene (CTTN). While cortactin overexpression enhances invasive potential, recent research indicates that it also promotes cell proliferation, but how cortactin regulates the cell cycle machinery is unclear. In this article we report that stable short hairpin RNA-mediated cortactin knockdown in the 11q13-amplified cell line FaDu led to increased expression of the Cip/Kip cyclin-dependent kinase inhibitors (CDKIs) p21(WAF1/Cip1), p27(Kip1), and p57(Kip2) and inhibition of S-phase entry. These effects were associated with increased binding of p21(WAF1/Cip1) and p27(Kip1) to cyclin D1- and E1-containing complexes and decreased retinoblastoma protein phosphorylation. Cortactin regulated expression of p21(WAF1/Cip1) and p27(Kip1) at the transcriptional and posttranscriptional levels, respectively. The direct roles of p21(WAF1/Cip1), p27(Kip1), and p57(Kip2) ...
The major findings in this study are that the Kip/Cip and Ink CKIs differentially regulate cdk2 and cdk4 in VSMCs; this, in turn, leads to differences in the inhibition of VSMC proliferation in vitro and in vivo. The expression of p27Kip1 and p21Cip1 in VSMCs inactivated cdk2 and cdk4, whereas p16Ink4 inhibited only cdk4 activity. In vivo, p27Kip1 significantly inhibited intimal cell proliferation and the development of a neointima after vascular injury, whereas p16Ink4 expression did not lead to a reduction in cell proliferation or neointima formation.. This different pattern of CKI inactivation of the CDKs suggests varied biological roles for p27Kip1 and p21Cip1 compared with p16Ink4 in VSMCs. p27Kip1 was initially characterized as an inhibitor of cyclin E/cdk2 phosphorylation.10 11 p27Kip1 and p21Cip1 are upregulated in several animal models of wound repair. p27Kip1 is constitutively expressed in normal arteries, is downregulated after arterial injury, and is upregulated during the later ...
We identified two patients with chromosomal abnormalities including SHOX trisomy by karyotype, one 9q22.3 microdeletion syndrome by CMA, two cases of Beckwith-Wiedemann syndrome by targeted MS-MLPA analysis and nine cases with heterozygous pathogenic or likely pathogenic genetic variants by multigene analysis techniques (FBN1 = 3, NSD1 = 2, NFIX = 1, SUZ12 = 1, CHD8 = 1, MC4R = 1). Three of 20 patients analyzed by WES had their diagnosis established. Only one non-syndromic patient had a definitive diagnosis. The sequential genetic assessment diagnosed 14 out of 42 (33.3%) tall patients. ...
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Natural History: Macroglossia and macrosomia are usually present at birth, although postnatal onset can occur. Neonatal hypoglycemia is common. Hemihyperplasia becomes more apparent as the child grows and may be limited to only one side of the body. Although cardiomegaly is common, it usually resolves on its own. Childhood malignancies and renal anomalies pose large health threats and mortality risks. After childhood, the complications for patients with BWS are infrequent ...
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Bastaki et al (2016) reported a case of BWS in a 9-year old Emirati boy. The patient was born to healthy, unrelated parents. He was found to have an omphalocele which contained small bowel and a small extra liver lobe. The patient was also found to suffer from cryptorchidism. Abdominal US revealed a non-progressive abdominal cyst. PCR amplification and sequencing of exons 2 and 3 of the CDKN1C gene identified a variant (c.703C,T) in the gene. According to in silico analysis results the protein change (p.Gln235X) leads to the production of a truncated protein that completely lacked the QT box. Polyphen 2 predicted that the variant was "probably damaging". The variant was not found in either of the parents DNA, marking it as a de novo mutation. ...
rs1063192 is a SNP in the cyclin-dependent kinase inhibitor 2B CDKN2B gene. A study of 432 Han Chinese patients with myocardial infarctions concluded that male subjects carrying a rs1063192(C) allele were at 0.71x decreased risk (for MI).[PMID 19272367] Myocardial Infarction ...
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begin{array}{*{20}c} {P_A = P_{total} X_A } \\ {\begin{array}{*{20}c} {where} & {X_A = \frac{{\begin{array}{*{20}c} {moles} & A \\ \end{array}}}{{\begin{array}{*{20}c} {total} & {moles} \\ \end{array}}}} \\ \end{array}} \\ \end{array ...
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Mammalian taste buds contain several specialized cell types that coordinately respond to tastants and communicate with sensory nerves. While it has long been appreciated that these cells undergo continual turnover, little is known concerning how adeq
Beckwith-Wiedemann syndrome is known as a genetic growth disorder that can causes large organs, large body size, and increase weight. The children who are
Mus musculus ATCC ® 63340™ Designation: CMV-p57 TypeStrain=False Application: in another host, produces protein cyclin-dependent kinase inhibitor 1C (p57, Kip2) P57, kinase inhibitory protein 2 of cyclins (p57)
CDKN2A / p14ARF antibody (cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4)) for ICC/IF, IHC, IHC-Fr, IHC-P, WB. Anti-CDKN2A / p14ARF pAb (GTX23642) is tested in Human samples. 100% Ab-Assurance.
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The timing of commitment and cell-cycle exit within progenitor populations during neurogenesis is a fundamental decision that impacts both the (...)
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BURBANK, Calif., April 11, 2017 /PRNewswire/ -- My Eye Media announced today that Kip Sears has joined the company in the newly created role of General Manager. Ive known Kip for many years and had the good fortune to work with him previously when we were both at Sony Pictures, said
def nearest_in_parent(start_element, condition_test): p = start_element.parent while p: for c in p.children: if condition_test(c): return c p = p.parent return None ...
Have you ever heard someone say that the cure is worse than disease? Or maybe, if the disease (whatever it may be) doesnt kill you the cure will? Sometimes, it does seem as if this is the .... ...
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 ... the mechanism by which p57 is able to affect such control is not yet known. Besides the ones listed above, there are several ...
"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". ...
... 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 ...
"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. PMC ... Meyerson M, Harlow E (Mar 1994). "Identification of G1 kinase activity for cdk6, a novel cyclin D partner". Molecular and ...
"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 ...
... (p57, Kip2), also known as CDKN1C, is 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 ... CDKN1C cyclin-dependent kinase inhibitor 1C (p57, Kip2)". Matsuoka S, Edwards MC, Bai C, Parker S, Zhang P, Baldini A, Harper ... Immuohistochemical stains for p57 can aid with the diagnosis of hydatidiform moles Cyclin-dependent kinase inhibitor 1C has ...
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 ...
CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... CDK4, CMM3, PSK-J3, cyclin-dependent kinase 4, cyclin dependent kinase 4. ... See also CDK inhibitor for inhibitors of various CDKs. Interactions[edit]. Cyclin-dependent kinase 4 has been shown to interact ... protein kinase activity. • kinase activity. • protein serine/threonine kinase activity. • cyclin-dependent protein serine/ ...
CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... "Identification of human cyclin-dependent kinase 8, a putative protein kinase partner for cyclin C". Proceedings of the National ... protein serine/threonine kinase activity. • cyclin-dependent protein serine/threonine kinase activity. ... The protein encoded by this gene is a member of the cyclin-dependent protein kinase (CDK) family. CDK8 and cyclin C associate ...
... 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 ... B-myb and selective members of cyclin/cdk subunits are targets for protein kinase C-mediated bimodal growth regulation in ...
Two key classes of regulatory molecules, cyclins and cyclin-dependent kinases (CDKs), determine a cell's progress through the ... The G1 cyclin-CDK complexes also promote the degradation of molecules that function as S phase inhibitors by targeting them for ... The cip/kip family includes the genes p21, p27 and p57. They halt cell cycle in G1 phase, by binding to, and inactivating, ... cyclin A, DNA polymerase, thymidine kinase, etc. Cyclin E thus produced binds to CDK2, forming the cyclin E-CDK2 complex, which ...
"Crystal structure of the p27Kip1 cyclin-dependent kinase inhibitor bound to the cyclin A-cdk2 complex". Nature. 382: 325-331. ... p57 can bind JNK1/SAPK, a stress-related kinase, and block its activity, protecting against JNK1-regulated apoptosis. CIP/KIP ... "Increased proteasome-dependent degredation of the cyclin-dependent kinase inhibitor p27 in aggressive colorectal carcinomas". ... As cyclin-dependent kinase inhibitors, CIP/KIP proteins have been classically viewed as tumor suppressors; however, the exact ...
... cyclin-dependent kinase inhibitor p27 MeSH D12.776.624.776.355.700 - cyclin-dependent kinase inhibitor p57 MeSH D12.776.664.235 ... 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 ...
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- ...
... *Cyclin-dependent kinase inhibitor protein. *Cyclin-dependent kinase. *Cyclin. Lipid. *Phosphoinositide phospholipase C ... CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... cyclin E, A (Cdk2,1) cyclin A, B, B3 (Cdk1) H. sapiens cyclin D 1,2,3 (Cdk4, Cdk6) cyclin E (Cdk2) cyclin A (Cdk2, Cdk1) cyclin ... Cyclin A / CDK2 - active in S phase.. *Cyclin D / CDK4, Cyclin D / CDK6, and Cyclin E / CDK2 - regulates transition from G1 to ...
All these phases in the cell cycle are highly regulated by cyclins, cyclin-dependent kinases, and other cell cycle proteins. ... CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... Generation of pressure is dependent on formin-mediated F-actin nucleation[71] and Rho kinase (ROCK)-mediated myosin II ... This can occur when cells become overcrowded (density-dependent inhibition) or when they differentiate to carry out specific ...
CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... April 2010). "Apoptosis induced by Oropouche virus infection in HeLa cells is dependent on virus protein expression". Virus Res ... Finally, the Akt protein kinase promotes cell survival through two pathways. Akt phosphorylates and inhibits Bas (a Bcl-2 ... Cyclin. *A (A1, A2). *B (B1, B2, B3). *D (D1, D2, D3) ... Using these inhibitors it was discovered that cells can die ...
CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... Cyclin. *A (A1, A2). *B (B1, B2, B3). *D (D1, D2, D3) ... CDK-activating kinase. ... "Predominant suppression of apoptosome by inhibitor of apoptosis protein in non-small cell lung cancer H460 cells: therapeutic ...
GTP-dependent protein binding. • GTPase activity. • mitogen-activated protein kinase kinase kinase binding. • protein binding. ... CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... Cyclin. *A (A1, A2). *B (B1, B2, B3). *D (D1, D2, D3) ... "The MAP kinase kinase kinase MLK2 co-localizes with activated ... protein kinase binding. • nucleotide binding. • GTP binding. • identical protein binding. Cellular component. • cytoplasm. • ...
Cyclin-dependent kinase 4,[30][31]. *Cyclin-dependent kinase inhibitor 1C,[32] ... "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- ...
cyclin-dependent kinase inhibitor 1C (P57). Synonyms: CDKI, Kip2, p57Kip2. Gene nomenclature, locus information, and GO, OMIM, ... OMIM: BECKWITH-WIEDEMANN SYNDROME; BWS, PREECLAMPSIA/ECLAMPSIA 1; PEE1, CYCLIN-DEPENDENT KINASE INHIBITOR 1C; CDKN1C, 614732* ...
P57(KIP2). Cyclin-dependent kinase inhibitor 1c. PI3K. Phosphatidylinositol 3-kinase. ProSAP2 (SHANK3). Proline-rich synapse- ...
The invention provides methods for assessing the efficacy of histone deacetylase inhibitors using biomarkers which can be used ... cyclin-dependent kinase. NM_000076. CDKN1C. inhibitor 1C (p57, Kip2). 2.8. superoxide dismutase 2,. AL050388;. SOD2. ... These include induction of cell cycle inhibitors such as the cyclin-dependent kinase inhibitor p21, induction of proapoptotic ... Plasminogen Activator Inhibitor-1 Inhibitors And Methods Of Use Thereof To Modulate Lipid Metabolism. January, 2009. Lawrence ...
... cyclin-dependent kinase inhibitor 1B; p57, cyclin-dependent kinase inhibitor 1C; c-Kit, kit oncogene; Myocd, myocardin; MRTF, ... The serine/threonine kinase Akt (also known as protein kinase B)/phosphoinositide-3 kinase (PI3K) signaling pathway plays a key ... NF-kappaB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses. Proc ... Ca2+/calmodulin kinase II-dependent regulation of atrial myocyte late Na+ current, Ca2+ cycling and excitability: a ...
... produces protein cyclin-dependent kinase inhibitor 1C (p57, Kip2) P57, kinase inhibitory protein 2 of cyclins (p57) ... CMV-p57 TypeStrain=False Application: in another host, ... cyclin-dependent kinase inhibitor 1C (p57, Kip2)(P57, kinase ... produces protein cyclin-dependent kinase inhibitor 1C (p57, Kip2) P57, kinase inhibitory protein 2 of cyclins (p57) ... CMV-p57 (ATCC® 63340™) Organism: Mus musculus, mouse / Clone Type: Clone / Depositors: SJ Elledge ...
tracked down the molecule that makes up this mitogen-dependent intracellular timer. The cyclin-dependent kinase inhibitor p57 ... Overexpression of p57Kip2 slowed the proliferation rate of OPCs in vitro to various degrees, depending on the availability of ... Thus, p57Kip2 fulfills the criteria for the primary component of this cellular clock, informing the cells when to abandon the ... Buildup of p57Kip2 also triggered expression of early gene markers of myelination. When the authors knocked down expression of ...
Oligodendrocyte precursor differentiation is perturbed in the absence of the cyclin-dependent kinase inhibitor p27Kip1. Genes ... A crucial role for p57(Kip2) in the intracellular timer that controls oligodendrocyte differentiation. J Neurosci. 2007;27(23): ... Age-dependent epigenetic control of differentiation inhibitors is critical for remyelination efficiency. Nat Neurosci. 2008;11( ... Olinone, an inhibitor the team developed against these bromodomains, increased OPC differentiation in cultured cells. They plan ...
Cyclin-Dependent Kinase Inhibitor 1C (CDKN1C) is a tumor suppressor; a protein involved in the regulation of cell division. ... Because it is a strong, tight inhibitor of several G1 cyclin/CDK complexes, this protein is a negative regulator of cell ...
Cyclin-dependent kinase inhibitor 1C (p57, Kip2), also known as CDKN1C, is 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 ... CDKN1C cyclin-dependent kinase inhibitor 1C (p57, Kip2)". Matsuoka S, Edwards MC, Bai C, Parker S, Zhang P, Baldini A, Harper ... Immuohistochemical stains for p57 can aid with the diagnosis of hydatidiform moles Cyclin-dependent kinase inhibitor 1C has ...
The activation of specific cyclin-dependent kinases (CDK) promotes cell proliferation. The cyclin-CDK complex is negatively ... regulated by CDK inhibitors p21, p27, and p57. Podocyte injury induces the loss of function of p27 and p57, resulting in ... The increased production of TGF-β might induce the expression of the integrin-linked kinase (ILK), a protein which is related ... Y. S. Kang, Y. Li, C. Dai, L. P. Kiss, C. Wu, and Y. Liu, "Inhibition of integrin-linked kinase blocks podocyte epithelial- ...
2007) The cyclin-dependent kinase inhibitors p57 and p27 regulate neuronal migration in the developing mouse neocortex. J Biol ... 2004) The cyclin-dependent kinase inhibitor p57(Kip2) mediates proliferative actions of PTHrP in chondrocytes. J Clin Invest ... Here, we report the discovery of such a molecule, the cyclin-dependent kinase inhibitor p57Kip2 (Cdkn1c). We show in vitro that ... 2001) Cyclin-dependent kinase inhibitors in the development of the central nervous system. Cell Growth Differ 12:387-396. ...
Cyclin dependent kinase inhibitor 1C (CDKN1C); Cyclin dependent kinase inhibitor p57; KIP2; p57; p57Kip2 ... Cloning of p57, a cyclin-dependent kinase inhibitor with unique domain structure and tissue distribution. Genes Dev. 9: 639-649 ... p57Kip2 is a potent tight-binding inhibitor of several G1 cyclin complexes, and is a negative regulator of cell proliferation. ... Anti-p57 has been used as an aide in identification of complete hydatidiform mole (CHM) (no nuclear labeling of ...
Cyclin-dependent Kinase Inhibitor p57KIP2 in Soft Tissue Sarcomas and Wilms Tumors ... Cyclin-dependent Kinase Inhibitor p57KIP2 in Soft Tissue Sarcomas and Wilms Tumors ... Cyclin-dependent Kinase Inhibitor p57KIP2 in Soft Tissue Sarcomas and Wilms Tumors ... Cyclin-dependent Kinase Inhibitor p57KIP2 in Soft Tissue Sarcomas and Wilms Tumors ...
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 ... the mechanism by which p57 is able to affect such control is not yet known. Besides the ones listed above, there are several ...
Li Y, Wang D, Zhang H, Wang C, Dai W, et al.. (2013) P21-Activated Kinase 4 Regulates the Cyclin-Dependent Kinase Inhibitor P57 ... The mRNA levels of USP22, BMI-1, p14ARF, c-Myc and cyclin D2, as well as that of the internal standard β-actin, were measured ... The results showed that USP22 was able to promote an increase in the endogenous concentration of c-Myc and cyclin D2 mRNA ( ... We examined the transcriptional relationship in the BMI-1, p14ARF, c-Myc and cyclin D2 expression by quantitative real-time PCR ...
Cloning of p57KIP2, a cyclin-dependent kinase inhibitor with unique domain structure and tissue distribution. Genes Dev, 9(6): ... Cloning of p27kip1, a cyclin-dependent kinase inhibitor and a potential mediator of extracellular antimitogenic signals. Cell, ... The p21 Cdkinteracting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases. Cell, 75(4):805-816. https://doi.org/ ... p27, a novel inhibitor of G1 cyclin-Cdk protein kinase activity, is related to p21. Cell, 78(1):67-74. https://doi.org/10.1016/ ...
cyclin-dependent kinase inhibitor 1C , cyclin-dependent kinase inhibitor p57 , cyclin-dependent kinase inhibitor 1C (p57, Kip2 ... Cyclin-Dependent Kinase Inhibitor 2B (p15, Inhibits CDK4) ELISA Kits * Cyclin-Dependent Kinase Inhibitor 2C (p18, Inhibits CDK4 ... Cyclin-Dependent Kinase 5, Regulatory Subunit 2 (p39) ELISA Kits * Cyclin-Dependent Kinase 5, Regulatory Subunit 1 (p35) ELISA ... cyclin-dependent kinase inhibitor 1Ca (cdkn1ca) ELISA Kit * cyclin-dependent kinase inhibitor 1C (P57) (Cdkn1c) ELISA Kit ...
2004). The cyclin-dependent kinase inhibitor p57 (Kip2) mediates proliferative actions of PTHrP in chondrocytes. J. Clin. ... 2000). Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1. Science 287, 664 ... and double-stranded RNA-activated protein kinase-likeendoplasmic reticulum kinase (PERK) in transcription during the mammalian ... H) Runx2-dependent transactivation of pATF6 gene was dramatically reduced when the Runx2-binding site was mutated (Mut1). The ...
CDKN1C encodes the protein p57KIP2, a member of the cyclin-dependent kinase inhibitor family which acts to negatively regulate ... A maternally inherited pathogenic variant in CDKN1C leading to increased stability of cyclin-dependent kinase inhibitor 1C was ... Oppositely imprinted genes p57(Kip2) and igf2 interact in a mouse model for Beckwith-Wiedemann syndrome. Genes Dev. 1999;13: ... Upregulation of Igf2 expression and downregulation of Cdkn1c (p57Kip2) result in phenotypes analogous to BWS in mouse models [ ...
... p57, Kip2)) for WB, IHC-Wm. Anti-Cdkn1c pAb (GTX54219) is tested in Zebrafish samples. 100% Ab-Assurance. ... cyclin-dependent kinase inhibitor 1C (p57, Kip2). Synonyms. cb961 Antibody , cdkn1c Antibody , cyclin-dependent kinase ...
Cyclin D- and E-dependent kinases and the p57(KIP2) inhibitor: cooperative interactions in vivo. Mol Cell Biol 1999; 19: 353-63 ... a pan cyclin-dependent kinase inhibitor, which has been shown to bind to and directly inhibit cyclin B1-CDC2 kinase, CDK2, CDK4 ... The universal CDI inhibitor Kip2 (p57, CDKN1C), which inhibits all of the G1 kinases (CDK2, CDK4, and CDK6), is 5-fold reduced ... The cyclin D-CDK4/6 for G1 progression ( 31), cyclin E-CDK2 for G1-S transition, cyclin A-CDK2 for S-phase progression ( 32), ...
Down-regulation of the cyclin-dependent kinase inhibitor p57 is mediated by Jab1/Csn5 in hepatocarcinogenesis. ...
Cyclin-dependent kinase inhibitors (CDKIs) play a critical role in negatively regulating the proliferation of cardiomyocytes, ... Stabilization of MyoD by direct binding to p57(Kip2)J Biol Chem 2000;275:18767-18776. [pmid: 10764802]. ... Cyclin-Dependent Kinase Inhibitor p27 / genetics, metabolism*. Gene Expression Regulation, Developmental. Heart / embryology*. ... Cyclin-dependent kinase inhibitor expression in human heart failure. A comparison with fetal developmentEur Heart J 1999;20:604 ...
A similar inhibitory effect on CDK9 was recently demonstrated for p57, a cyclin-dependent kinase inhibitor closely related to ... on how the cyclin-dependent kinase inhibitor p21 can block HIV-1 replication by interfering with cyclin-dependent kinase 9 ( ... Other members of the family of cyclin-dependent kinase inhibitors, such as p27 or p57, were not differentially expressed in CD4 ... Inhibition of human immunodeficiency virus type 1 transcription by chemical cyclin-dependent kinase inhibitors. J Virol. 2001; ...
... p57, Kip2) (CDKN1C), transcript variant 1 as transfection-ready DNA available for purchase from OriGene - Your Gene Company. ... Myc-DDK-tagged ORF clone of Homo sapiens cyclin-dependent kinase inhibitor 1C ( ... Mouse cyclin-dependent kinase inhibitor 1C (P57) (Cdkn1c). $430. 3 weeks. MG227583. Cdkn1c (GFP-tagged) - Mouse cyclin- ... Cdkn1c (untagged) - Mouse cyclin-dependent kinase inhibitor 1C (P57) (Cdkn1c), transcript variant 1, (10ug). $390. Next day. ...
  • The presence of two families of seven distinct mammalian cyclin-dependent kinase (CDK) inhibitor genes is thought to mediate the complexity of connecting a variety of cellular processes to the cell cycle control pathway. (asm.org)
  • The distinct pattern of tissue expression of CDK inhibitor genes suggests that they may function as tumor suppressors with different tissue specificities. (asm.org)
  • Our results suggest that functional collaborations between distinct CDK inhibitor genes are tissue specific and confer yet another level of regulation in cell growth control and tumor suppression. (asm.org)
  • Two families of cyclin-dependent kinase (CDK) inhibitors, totaling seven genes, have been identified in mammalian cells. (asm.org)
  • Their similar biochemical activity in blocking CDK enzymes and maintaining the growth-suppressive activity of Rb predict a tumor suppression function for CDK inhibitor genes, yet only the p16 INK4a gene has been directly linked to tumor growth by genetic alterations found in human cancers ( 17 , 25 ) and by the early development of spontaneous tumors in mice lacking p16 ( 31 ). (asm.org)
  • Neither mutational analysis in human tumors nor phenotypic examination of genetically targeted mice lacking any of the other individual CDK inhibitor genes has provided strong evidence for a direct role for any of the other CDK inhibitors as tumor suppressors. (asm.org)
  • Rb inactivation leads to expression of E2F-dependent genes such as thymidine kinase, DNA polymerase-α, cdc2, and cyclin A ( 5 ), which are not expressed in senescent cells ( 6 ), indicating that the failure to phosphorylate Rb is important in the growth arrest of senescent cells. (pnas.org)
  • First, we found that the IRAK4 kinase activity was required for modified LDL-induced NF-κB activation and expression of a subset of proinflammatory genes but not for the activation of MAPKs in bone marrow-derived macrophage. (jimmunol.org)
  • Hoxa-10 mutants express a stromal cell proliferation defect that is accompanied by quantitative or spatial alterations in the expression of two cyclin-dependent kinase inhibitor genes, p57 and p15. (broadinstitute.org)
  • A previous screen of a human kinase and phosphatase shRNA library to select genes that mediate arsenite induction of spindle abnormalities resulted in the identification of phosphatidylinositol-5-phosphate 4-k. (biomedcentral.com)
  • Taken together, our results indicate that the IRAK4 kinase plays an important role in modified LDL-mediated signaling and the development of atherosclerosis, suggesting that pharmacological inhibition of IRAK4 kinase activity might be a feasible approach in the development of antiatherosclerosis drugs. (jimmunol.org)
  • Vikram, we are aware of many studies that show that inhibition of Cdk5 using pharmacological inhibitors or DNK5 can be neuroprotective, for example, in ischemia. (alzforum.org)
  • Employing an organ culture system of embryonic mouse tibiae and LY294002, a pharmacological inhibitor of PI3K, we show that inhibition of the pathway results in significant growth reduction, demonstrating that PI3K is required for normal endochondral bone growth in vitro . (biomedcentral.com)
  • GSK-3 inhibition rescues some effects of phosphatidylinositide 3-kinase inhibition in this system, in agreement with the antagonistic role of these two kinases in response to signals such as IGF. (heightquest.com)
  • In tibia organ culture, inhibition of GSK-3 or dual treatments of GSK-3 and PI3K inhibitors greatly increased the zone of p57 protein expression in the prehypertrophic zone" "up-regulation of GSK-3α compensates for the loss of GSK-3β in cartilage. (heightquest.com)
  • In a corollary in vivo study, YC-1 induced dose-dependent inhibition of tumor growth in mice inoculated with HA22T cells. (aspetjournals.org)
  • In addition, our data indicated that SKP2 promotes anoikis resistance through the phosphoinositidyl 3-kinase (PI3K)-Akt pathway. (aacrjournals.org)
  • As one example, we have only recently learned that loss of the platelet-derived growth factor (PDGF) receptor-α in adult human β-cells, with the resultant loss of ability to activate mitogen-activated protein kinase and methylation (Ezh2) and downstream cell cycle (p16) machinery, may underlie the refractoriness of human β-cells to proliferation ( 16 ). (diabetesjournals.org)
  • It was further shown that cGMP, p42/p44 mitogen-activated protein kinase, or AKT kinase-mediated signaling pathways did not contribute to the YC-1-induced effect. (aspetjournals.org)
  • Overexpression of any of the cdk inhibitors will induce G1-cell cycle arrest [ 3 ]. (biomedcentral.com)
  • Overexpression of p57 Kip 2 has been previously shown to prevent apoptotic cell death in vitro by inhibiting stress-activated kinases. (biomedcentral.com)
  • Transgenic mice with cardiac specific overexpression of p57 Kip 2 are viable, fertile and normally active and their hearts are morphologically indistinguishable from the control hearts and have similar heart weight/body weight ratio. (biomedcentral.com)
  • To investigate the role of P16 (INK4a)-extracellular signal related kinase 1/2 (ERK1/2) signaling pathway in cisplatin (DDP) resistance induced by multidrug resistance protein 1 (MDR1), also known as P-glycopr. (biomedcentral.com)
  • The INK4 family consists of p16 INK4a , p15 INK4b , p18 INK4c , and p19 INK4d , which narrow specifically to form stale complexes with CDK4/6 before binding with cyclin D ( Vidal and Koff, 2000 ). (aspetjournals.org)
  • IRAK4 kinase-inactive knockin (IRAK4KI) mice were bred onto ApoE −/− mice to generate IRAK4KI/ApoE −/− mice. (jimmunol.org)
  • The TKO embryos manifested morphological abnormalities as well as increased rates of cell proliferation and apoptosis in the placenta and lens that were essentially indistinguishable from those of p27/p57 DKO mice. (elsevier.com)
  • This indicates that an increase in G 1 CDK kinase activity is a critical step during but is not sufficient for tumor growth. (asm.org)
  • In this study, we examined the role of IL-1R-associated kinase 4 (IRAK4) kinase activity in modified low-density lipoprotein (LDL)-mediated signaling using bone marrow-derived macrophage as well as an in vivo model of atherosclerosis. (jimmunol.org)
  • It is a bifunctional signaling molecule that controls serine/threonine kinase and serine/threonine phosphatase activity (2). (cellsignal.com)
  • 1994). Hunter T: p27, a novel inhibitor of G1 cyclin-Cdk protein kinase activity, is related to p21. (core.ac.uk)
  • At the molecular level, lack of FBL17 increases the stability of the CDK (CYCLIN-DEPENDENT KINASE) inhibitor KIP-RELATED PROTEIN2 known to switch off CDKA;1 kinase activity. (plantcell.org)
  • Recent work exploring p21 activation in response to DNA damage at a single-cell level have demonstrated that pulsatile p53 activity leads to subsequent pulses of p21, and that the strength of p21 activation is cell cycle phase dependent. (wikipedia.org)
  • Three signaling pathways are involved in the UPR, and these are mediated by inositol-requiring enzyme-1 (IRE1, also known as ERN1), PKR-like ER resistant kinase (PERK, also known as EIF2AK3) and activation transcription factor 6 (ATF6), which act in concert to limit new protein synthesis and to increase the levels of chaperones. (biologists.org)
  • Interestingly, the proliferation markers nuclear transcription factor p63 and cyclin D1 were upregulated, while cyclin-dependent kinase inhibitor p57 was downregulted at both mRNA and protein levels. (arvojournals.org)
  • Complete hydatidiform moles consist only of paternal DNA, and thus the cells lack p57 expression as the gene is paternally imprinted (silenced). (wikipedia.org)
  • The figure shows one of the characterized processing patterns of the PTH rP preprohormone, resulting in three bioactive peptides: the N-terminal homologous to PTH, the midregion PTH rP that augments calcium transport and the C-terminal peptide, Osteostatin , that is a potent inhibitor of bone resorption. (diff.org)
  • Consistently, deletion of PKD1 promotes expression of the β3-adrenergic receptor (ADRB3) in a CCAAT/enhancerbinding protein (C/EBP)-α and δ-dependent manner, which leads to the elevated expression of beige markers in adipocytes and subcutaneous adipose tissue. (uni-wuerzburg.de)
  • Outside of G 0 , the MuvB core also binds b-Myb and FoxM1 to drive relevant cell-cycle-dependent gene expression ( 14 ). (aacrjournals.org)
  • We demonstrated previously that expression of the cell cycle inhibitor p21 is significantly reduced in RA synovial lining, particularly in the FLS. (biomedcentral.com)
  • Different cyclins exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. (wikidoc.org)
  • 2001). Chemopreventive effects of green tea polyphenols correlate with reversible induction of p57 expression. (core.ac.uk)
  • Our results show that miR-221 and miR-222 both directly target the 3' untranslated regions of p27 and p57 mRNAs to reduce reporter gene expression, as well as diminish p27 and p57 protein levels. (umassmed.edu)
  • expression of cyclin D1, D2, and cyclin E showed little change. (elsevier.com)