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

Comparative molecular genetic profiles of anaplastic astrocytomas/glioblastomas multiforme and their subsequent recurrences. (1/401)

Malignant glial tumors (anaplastic astrocytomas and glioblastomas multiforme) arise mostly either from the progression of low grade precursor lesions or rapidly in a de novo fashion and contain distinct genetic alterations. There is, however, a third subset of malignant gliomas in which genetic lesions remain to be identified. Following surgical resection, all gliomas appear to have an inherent tendency to recur. Comparative molecular analysis of ten primary malignant gliomas (three anaplastic astrocytomas and seven glioblastomas multiforme) with their recurrences identified two distinct subgroups of recurrent tumors. In one group, primary tumors harbored genetic aberrations frequently associated with linear progression or de novo formation pathways of glial tumorigenesis and maintained their genetic profiles upon recurrence. In the other subset with no detectable known genetic mutations at first presentation, the recurrent tumors sustained specific abnormalities associated with pathways of linear progression or de novo formation. These included loss of genes on chromosomes 17 and 10, mutations in the p53 gene, homozygous deletion of the DMBTA1 and p16 and/ or p15 genes and amplification and/or overexpression of CDK4 and alpha form of the PDGF receptor. Recurrent tumors from both groups also displayed an abnormal expression profile of the metalloproteinase, gel A, and its inhibitor, TIMP-2, consistent with their highly invasive behavior. Delineation of the molecular differences between malignant glioblastomas and their subsequent recurrences may have important implications for the development of rational clinical approaches for this neoplasm that remains refractory to existing therapeutic modalities.  (+info)

Cyclin D-CDK subunit arrangement is dependent on the availability of competing INK4 and p21 class inhibitors. (2/401)

The D-type cyclins and their major kinase partners CDK4 and CDK6 regulate G0-G1-S progression by contributing to the phosphorylation and inactivation of the retinoblastoma gene product, pRB. Assembly of active cyclin D-CDK complexes in response to mitogenic signals is negatively regulated by INK4 family members. Here we show that although all four INK4 proteins associate with CDK4 and CDK6 in vitro, only p16(INK4a) can form stable, binary complexes with both CDK4 and CDK6 in proliferating cells. The other INK4 family members form stable complexes with CDK6 but associate only transiently with CDK4. Conversely, CDK4 stably associates with both p21(CIP1) and p27(KIP1) in cyclin-containing complexes, suggesting that CDK4 is in equilibrium between INK4 and p21(CIP1)- or p27(KIP1)-bound states. In agreement with this hypothesis, overexpression of p21(CIP1) in 293 cells, where CDK4 is bound to p16(INK4a), stimulates the formation of ternary cyclin D-CDK4-p21(CIP1) complexes. These data suggest that members of the p21 family of proteins promote the association of D-type cyclins with CDKs by counteracting the effects of INK4 molecules.  (+info)

p53 and p16INK4A mutations during the progression of glomus tumor. (3/401)

Glomus tumors are significantly rare tumors of carotid body. The great majority of these tumors are benign in character. Here we present two brothers with hereditary glomus jugulare tumor who had consanguineous parents. Radiotherapy was applied approximately 8 and 10 years ago for treatment in both cases. Eight years later, one of these cases came to our notice due to relapse. The mutation pattern of p53, p57KIP2, p16INK4A and p15NK4B genes which have roles in the cell cycle, was analyzed in tumor samples obtained from the two affected cases in the initial phase and from one of these cases at relapse. The DNA sample obtained from the case in initial diagnosis phase revealed no p53, p57KIP2, p16INK4A or p15INK4B mutation. He is still in remission phase. Despite the lack of p53, p57KIP2, p16INK4A and p15INK4B mutation at initial diagnosis the tumor DNA of the other case in relapse revealed p53 codon 243 (ATG-->ATC; met-->ile) and p16 codon 97 (GAC-->AAC; asp-->asn) missense point mutations. No loss of heterozygosity in p53 and p16INK4A was observed by microsatellite analysis of tumoral tissues in these cases. P53 and p16INK4A mutations observed in relapse phase were in conserved regions of both genes. No previous reports have been published with these mutations in glomus tumor during progression. The mutation observed in this case may due to radiotherapy. In spite of this possibility, the missense point mutations in conserved region of p53 and p16INK4A genes may indicate the role of p53 and p16INK4A in tumor progression of glomus tumors.  (+info)

Acquisition of p16(INK4A) and p15(INK4B) gene abnormalities between initial diagnosis and relapse in children with acute lymphoblastic leukemia. (4/401)

Although numerous somatic mutations that contribute to the pathogenesis of childhood acute lymphoblastic leukemia (ALL) have been identified, no specific cytogenetic or molecular abnormalities are known to be consistently associated with relapse. The p16(INK4A) (p16), which encodes for both p16(INK4A) and p19(ARF) proteins, and p15(INK4B) (p15) genes are inactivated by homozygous deletion and/or p15 promoter hypermethylation in a significant proportion of cases of childhood ALL at the time of initial diagnosis. To determine whether alterations in these genes play a role in disease progression, we analyzed a panel of 18 matched specimen pairs collected from children with ALL at the time of initial diagnosis and first bone marrow relapse for homozygous p16 and/or p15 deletions or p15 promoter hypermethylation. Four sample pairs contained homozygous p16 and p15 deletions at both diagnosis and relapse. Among the 14 pairs that were p16/p15 germline at diagnosis, three ALLs developed homozygous deletions of both p16 and p15, and two developed homozygous p16 deletions and retained p15 germline status at relapse. In two patients, p15 promoter hypermethylation developed in the interval between initial diagnosis and relapse. In total, homozygous p16 deletions were present in nine of 18 cases, homozygous p15 deletions in seven of 18 cases, and p15 promoter hypermethylation in two of eight cases at relapse. These findings indicate that loss of function of proteins encoded by p16 and/or p15 plays an important role in the biology of relapsed childhood ALL, and is associated with disease progression in a subset of cases.  (+info)

INK4 cell cycle inhibitors direct transcriptional inactivation of NF-kappaB. (5/401)

The nuclear factor kappaB, a transcription factor regulating the expression of multiple genes including genes essential for cell cycle control, is found in most cells in a dormant state in the cytoplasm bound to the inhibitory family I kappaB via an ankyrin repeat domain. Stimulation of cells with a variety of inducers inactivates I kappaB proteins. The active dimeric NF-kappaB complex, often composed of 50- and 65-kilodalton subunits of the Rel family, translocates into the nucleus, where the NF-kappaBp65 subunit stimulates transcription. Here we report that a family of proteins containing ankyrin repeats, the inhibitors of Cdk4 (INK4) is able to bind NF-kappaBp65. The association of p16INK4 with NF-kappaBp65 is considerable in HeLa- or 293 cells, if the NF-kappaB inhibitor I kappaB alpha is degraded in response to TNFalpha stimulation. Overexpression of INK4 molecules suppresses the transactivational ability of NF-kappaB significantly. In contrast to INK4 proteins, the cell cycle inhibitor p27 enhances NF-kappaB transactivation activity. Thus, the effect of INK4 proteins on NF-kappaB function possibly modifies NF-kappaB mediated transcriptional activation of cell cycle associated factors.  (+info)

Molecular mechanisms underlying interferon-alpha-induced G0/G1 arrest: CKI-mediated regulation of G1 Cdk-complexes and activation of pocket proteins. (6/401)

One prominent effect of IFNs is their cell growth-inhibitory activity. The mechanism behind this inhibition of proliferation is still not fully understood. In this study, the effect of IFN-alpha treatment on cell cycle progression has been analysed in three lymphoid cell lines, Daudi, U-266 and H9. Examination of the growth-arrested cell populations shows that Daudi cells accumulate in a G0-like state, whereas U-266 cells arrest later in G1. H9 cells are completely resistant to IFN-alpha's cell growth-inhibitory effects. The G0/G1-phase arrest is preceded by a rapid induction of the cyclin-dependent kinase inhibitors (CKIs), p21 and p15. In parallel, the activities of the G1 Cdks are significantly reduced. In addition to p21/p15 induction, IFN-alpha regulates the expression of another CKI, p27, presumably by a post-transcriptional mechanism. In the G1 Cdk-complexes, there is first an increased binding of p21 and p15 to their respective kinases. At longer exposure times, when Cdk-bound p15 and p21 decline, p27 starts to accumulate. Furthermore, we found that IFN-alpha not only suppresses the phosphorylation of pRb, but also alters the phosphorylation and expression of the other pocket proteins p130 and p107. These data suggest that induction of p21/p15 is involved in the primary IFN-alpha response inhibiting G1 Cdk activity, whereas increased p27 expression is part of a second set of events which keep these Cdks in their inactive form. Moreover, elevated levels of p27 correlated with a dissociation of cyclin E/Cdk2-p130 or p107 complexes to yield cyclin E/Cdk2-p27 complexes. In resistant H9 cells, which possess a homozygous deletion of the p15/p16 genes and lack p21 protein expression, IFN-alpha causes no detectable changes in p27 expression and, furthermore, no effects are observed on either pocket proteins in this cell line. Taken together, these data suggest that the early decline in G1 Cdk activity, subsequent changes in phosphorylation of pocket proteins, and G1/G0 arrest following IFN-alpha treatment, is not primarily due to loss of the G1 kinase components, but result from the inhibitory action of CKIs on these complexes.  (+info)

Acceleration of c-myc-induced hepatocarcinogenesis by Co-expression of transforming growth factor (TGF)-alpha in transgenic mice is associated with TGF-beta1 signaling disruption. (7/401)

We have previously shown in transgenic mice that transforming growth factor (TGF)-alpha dramatically enhances c-myc-induced hepatocarcinogenesis by promoting proliferation and survival of hepatocellular carcinoma (HCC) cells. As transgenic livers display increased levels of mature TGF-beta1 from the early stages of hepatocarcinogenesis, we have now assessed whether impairment of TGF-beta1 signaling contributes to the deregulation of cell cycle progression and apoptosis observed during this process. Focal preneoplastic lesions lacking expression of TGF-beta receptor type II (TbetaRII) were detected in c-myc/TGF-alpha but not in c-myc livers. In c-myc/TGF-alpha mice, 40% (2/5) of adenomas and 90% (27/30) of HCCs showed down-regulation of TbetaRII expression in comparison with 11% (2/18) of adenomas and 47% (14/30) of HCCs in c-myc mice. Down-regulation of the TGF-beta1-inducible p15(INK4B) mRNA and reduced apoptotic rates in TbetaRII-negative HCCs further indicated the disruption of TGF-beta1 signaling. Furthermore, both TbetaRII-negative and -positive c-myc TGF-alpha HCCs, but not c-myc HCCs, were characterized by decreased levels of the cell cycle inhibitor p27. These results suggest 1) an inverse correlation of decreased p27 expression with the particularly strong expression of TGF-alpha in these lesions, consistent with the capacity of TGF-alpha signaling to post-transcriptionally regulate p27, and 2) the presence of alternative, downstream defects of TGF-beta1 signaling in c-myc/TGF-alpha HCCs that may impair the growth-inhibitory response to TGF-beta1. Thus, the accelerated neoplastic development in c-myc/TGF-alpha mice is associated with an early and frequent occurrence of TbetaRII-negative lesions and with reduced levels of p27 in HCC cells, indicating that disruption of TGF-beta1 responsiveness may play a crucial role in the enhancement of c-myc-induced hepatocarcinogenesis by TGF-alpha.  (+info)

TaqMan PCR-based gene dosage assay for predictive testing in individuals from a cancer family with INK4 locus haploinsufficiency. (8/401)

BACKGROUND: A genetic syndrome of cutaneous malignant melanoma and nervous system tumors recently has been characterized and shown to be linked to the INK4 locus in the 9p21 region. Hemizygosity at adjacent physically mapped microsatellite markers indicated deletion of p16, p19, and p15 clustered tumor suppressors. Because individuals from this family could benefit from predictive testing in terms of cancer prevention, we developed a direct test without need to analyze parental DNAs to comply with the rules of individual consent and secrecy. METHODS: We developed an assay using TaqManTM real-time quantitative PCR, with p15 as the test sequence and albumin (ALB) as the reference gene. The normalized ratio of p15/ALB is expected to yield a value of approximately 1 in individuals without the deletion, whereas a ratio of approximately 0.5, indicating p15 haploinsufficiency, is expected in predisposed individuals. RESULTS: All patients harboring the previously defined at-risk haplotype were correctly identified using this approach. In six individuals with deletions, the p15/ALB ratios were 0.472-0.556 (SD, 0.013-0.078). In the five individuals without deletions, the ratios were 0.919-1.019 (SD, 0.006-0.075). CONCLUSIONS: This is the first report of a high-throughput, automatable gene dosage assay successfully applied to the identification of a germ-line deletion. This approach, not limited by marker informativeness or the need for harvesting live cells, can be applied to any condition with haploinsufficiency and extended to the characterization of most abnormalities of the ploidy.  (+info)

*CDKN2B

"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... "Entrez Gene: CDKN2B cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4)". Rual JF, Venkatesan K, Hao T, Hirozane- ... an alternatively spliced form of p15 cyclin-dependent kinase inhibitor". Cancer Res. 57 (14): 2966-73. PMID 9230210. Rich JN, ... Cyclin-dependent kinase 4 inhibitor B also known as multiple tumor suppressor 2 (MTS-2) or p15INK4b is a protein that is ...

*Cyclin-dependent kinase 4

"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... See also CDK inhibitor for inhibitors of various CDKs. Cyclin-dependent kinase 4 has been shown to interact with: CDC37, CDKN1B ... 1995). "Identification of human cyclin-dependent kinase 8, a putative protein kinase partner for cyclin C". Proc. Natl. Acad. ... "The nuclear protein p34SEI-1 regulates the kinase activity of cyclin-dependent kinase 4 in a concentration-dependent manner". ...

*Cyclin A1

"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... Cyclins function as activating subunits of enzymatic complex together with cyclin-dependent kinases (CDKs). Different cyclins ... and the Kip/Cip family of CDK-inhibitor proteins. Cyclin-A1 interacts with: CDC20, Cyclin-dependent kinase 2, E2F1, GNB2L1, ... cyclins and cyclin dependent kinases". Oncogene. 15 (2): 143-57. doi:10.1038/sj.onc.1201252. PMID 9244350. Suzuki Y, Yoshitomo- ...

*Cyclin D

Inactivation of cyclin D is triggered by several cyclin-dependent kinase inhibitor protein (CKIs) like the INK4 family (e.g. ... p14, p15, p16, p18). INK4 proteins are activated in response to hyperproliferative stress response that inhibits cell ... activate cyclin D gene in response to integrin. p27kip1 and p21cip1 are cyclin-dependent kinase inhibitors (CKIs) which ... Cyclins are eukaryotic proteins that form holoenzymes with cyclin-dependent protein kinases (Cdk), which they activate. The ...

*Cyclin D1

"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... Hall M, Peters G (1996). "Genetic alterations of cyclins, cyclin-dependent kinases, and Cdk inhibitors in human cancer". ... Cyclins function as regulators of CDKs (Cyclin-dependent kinase). Different cyclins exhibit distinct expression and degradation ... cyclin box domain for cyclin-dependent kinase (CDK) binding and CDK inhibitor binding; LxxLL binding motif for co-activator ...

*Cyclin-dependent kinase 6

Furthermore, inhibitors of the INK4 family members like p15, p16, p18 and p19 inhibit the monomer of CDK6, preventing the ... "Both p16 and p21 families of cyclin-dependent kinase (CDK) inhibitors block the phosphorylation of cyclin-dependent kinases by ... It is regulated by cyclins, more specifically by Cyclin D proteins and Cyclin-dependent kinase inhibitor proteins. The protein ... 2003). "Expression of Cyclin-Dependent Kinase 6, but Not Cyclin-Dependent Kinase 4, Alters Morphology of Cultured Mouse ...

*Flap structure-specific endonuclease 1

... and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21". J. Biol. Chem. ... Yu P, Huang B, Shen M, Lau C, Chan E, Michel J, Xiong Y, Payan DG, Luo Y (Jan 2001). "p15(PAF), a novel PCNA associated factor ... and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21". J. Biol. Chem. ... Henneke G, Koundrioukoff S, Hübscher U (Jul 2003). "Phosphorylation of human Fen1 by cyclin-dependent kinase modulates its role ...

*CDKN2A

"CDKN2A cyclin dependent kinase inhibitor 2A [Homo sapiens (human)] - Gene - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2016-10-11. ... Kanellou P, Zaravinos A, Zioga M, Spandidos DA (June 2009). "Deregulation of the tumour suppressor genes p14(ARF), p15(INK4b), ... CDKN2A, also known as cyclin-dependent kinase Inhibitor 2A, is a gene which in humans is located at chromosome 9, band p21.3. ... "CDKN2A - Cyclin-dependent kinase inhibitor 2A - Homo sapiens (Human) - CDKN2A gene & protein". www.uniprot.org. Retrieved 2016- ...

*Proliferating cell nuclear antigen

Cyclin D1, Cyclin O, Cyclin-dependent kinase 4, Cyclin-dependent kinase inhibitor 1C, DNMT1, EP300, Flap structure-specific ... Yu P, Huang B, Shen M, Lau C, Chan E, Michel J, Xiong Y, Payan DG, Luo Y (January 2001). "p15(PAF), a novel PCNA associated ... "A small peptide inhibitor of DNA replication defines the site of interaction between the cyclin-dependent kinase inhibitor ... and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21". J. Biol. Chem. ...

*P21

... also known as cyclin-dependent kinase inhibitor 1 or CDK-interacting protein 1, is a cyclin-dependent kinase inhibitor (CKI) ... Yu P, Huang B, Shen M, Lau C, Chan E, Michel J, Xiong Y, Payan DG, Luo Y (January 2001). "p15(PAF), a novel PCNA associated ... "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 ...

*Transforming growth factor beta

... inducing expression of cyclin-dependent kinase inhibitor 21 (a regulator of cell cycle progression through the G1 and S phase ... TGF-β causes synthesis of p15 and p21 proteins, which block the cyclin:CDK complex responsible for retinoblastoma protein (Rb) ... After the binding of TGF-β, the type 2 receptor kinase phosphorylates and activates the type 1 receptor kinase that activates a ... which then activates apoptosis signal-inducing kinase 1 (ASK1), which goes on to activate the Jun amino-terminal kinase (JNK) ...

*PFKFB3

"Nuclear Targeting of 6-Phosphofructo-2-kinase (PFKFB3) Increases Proliferation via Cyclin-dependent Kinases". Journal of ... Boyd, Scott (April 7, 2015). "Structure-Based Design of Potent and Selective Inhibitors of the Metabolic Kinase PFKFB3". J. Med ... "The third human isoform of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3) map position 10p14-p15". Chromosome ... and suppresses apoptosis by regulating cyclin-dependent kinase 1 (Cdk-1). PFKFB3's synthesis of F2,6BP in the nucleus was found ...

*List of MeSH codes (D12.776)

... 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 inhibitor p21 MeSH D12.776.624.776.355.600 - cyclin-dependent kinase inhibitor p27 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 8

The natural product cortistatin A is a potent and selective inhibitor of CDK8 and CDK19. Inhibition of CDK8 and CDK19 with ... Vogel L, Baratte B, Détivaud L, Azzi L, Leopold P, Meijer L (Apr 2002). "Molecular cloning and characterisation of p15(CDK-BP ... "Identification of human cyclin-dependent kinase 8, a putative protein kinase partner for cyclin C". Proceedings of the National ... The protein encoded by this gene is a member of the cyclin-dependent protein kinase (CDK) family. CDK8 and cyclin C associate ...

*Long non-coding RNA

Yik JH, Chen R, Nishimura R, Jennings JL, Link AJ, Zhou Q (October 2003). "Inhibition of P-TEFb (CDK9/Cyclin T) kinase and RNA ... The existence of an RNAP III-dependent ncRNA transcriptome that regulates its RNAP II-dependent counterpart was supported by a ... was able to induce changes to heterochromatin and DNA methylation status of p15 by an unknown mechanism, thereby regulating p15 ... Liu WM, Chu WM, Choudary PV, Schmid CW (May 1995). "Cell stress and translational inhibitors transiently increase the abundance ...

*Myc

Expression of Myc is highly dependent on BRD4 function in some cancers. BET inhibitors have been used to successfully block Myc ... "Mitogen-activated protein kinase kinase 7 is an activator of the c-Jun NH2-terminal kinase". Proceedings of the National ... "Direct interaction of c-Myc with Smad2 and Smad3 to inhibit TGF-beta-mediated induction of the CDK inhibitor p15(Ink4B)". ... Myc has been shown to interact with: ACTL6A BRCA1 Bcl-2 Cyclin T1 CHD8 DNMT3A EP400 GTF2I HTATIP let-7 MAPK1 MAPK8 MAX MLH1 ...
Recent studies suggest that ANRIL expression mediates susceptibility to CAD1 via CDKN2B.2 We used fluorescently-labelled whole-blood RNA, from 20 healthy volunteers genotyped for the CAD-risk-SNP rs2891168, to probe custom-designed Agilent tiling expression microarrays. Raw data were normalized to probe GC content and housekeeping genes. We found that ANRIL exons 1-4 were more abundantly expressed in blood than 5-20, with exons 6, 8, 9, 20 showing low expression. We derived a set of "training" tiling probes from HUVEC cells in which ANRIL expression was attenuated using siRNA against exons 13 and 19. ANRIL expression (probes in exons 5,6,8,13,16,18,19) was reduced by at least 50% and CDKN2B expression (probes in exons 1,2) increased, with no effect on CDKN2A. We confirmed these data using real-time QPCR. Using the tiling probe "training-set", a probe in exon 16 of ANRIL showed a CAD genotype-specific difference in expression (p,0.001), with the risk-allele lower, and probes in exon 2 of CDKN2B ...
Results In the global gene expression analysis, we found strong cis eQTLs for both CDKN2B (p=1.3×10−38) and MTAP (p=6.6×10−23), explaining 17.0% and 8.0% of the expression of these genes. AE analysis confirmed these findings (CDKN2B, p=6.0×10−64; MTAP, p=1.4×10−38) and also showed a significant cis-eQTL effect on ANRIL expression (p=3.5×10−28). Interestingly, the SNPs associated with CDKN2B and ANRIL expression were the same. However, the SNPs showing e-QTL effects were distinct from SNPs that showed an association with CAD risk (p=2.2×10−12). Even in the region with a physical overlap of variants affecting expression of CDKN2B/ANRIL and CAD risk, the effects of the respective variants were independent of each other. Expression of CDKN2A and ARF was low but did not show any obvious eQTL effect, or differences according to genotype at CAD-associated SNPs. ...
Hepatocellular carcinoma (HCC) is a common malignant tumor with high fatality rate. Recent studies reported that up-regulation of long non-coding RNA antisense non-coding RNA in the INK4 locus (lncRNA ANRIL) was found in HCC tissues, and which could affect HCC cells biological processes. However, the potential molecular mechanism of ANRIL in HCC is still unclear. The study aimed to uncover the effect of ANRIL on HepG2 cells growth, migration and invasion. The knockdown expression vectors of ANRIL were transfected into HepG2 cells, and qRT-PCR, CCK-8, flow cytometry, Transwell and western blot assays were performed to analyze the effect of ANRIL on cell proliferation, apoptosis, migration and invasion. The relative expression of miR-191 was then examined in ANRIL knockdown vector transfected cells. These experiments were repeated again for exploring the effect of miR-191 on HepG2 cells. NF-κB and Wnt/β-catenin signaling pathways were examined by using western blot assay. Knockdown of ANRIL inhibited
TY - JOUR. T1 - Restricted heterochromatin formation links NFATc2 repressor activity with growth promotion in pancreatic cancer. AU - Baumgart, Sandra. AU - Glesel, Elisabeth. AU - Singh, Garima. AU - Chen, Naiming. AU - Reutlinger, Kristina. AU - Zhang, Jinsan. AU - Billadeau, Daniel D. AU - Fernandez-Zapico, Martin E. AU - Gress, Thomas M.. AU - Singh, Shiv K.. AU - Ellenrieder, Volker. PY - 2012/2. Y1 - 2012/2. N2 - Background & Aims: Transcriptional silencing of the p15 INK4b tumor suppressor pathway overcomes cellular protection against unrestrained proliferation in cancer. Here we show a novel pathway involving the oncogenic transcription factor nuclear factor of activated T cells (NFAT) c2 targeting a p15 INK4b-mediated failsafe mechanism to promote pancreatic cancer tumor growth. Methods: Immunohistochemistry, real-time polymerase chain reaction, immunoblotting, and immunofluorescence microscopy were used for expression studies. Cancer growth was assessed in vitro by [ 3H] thymidine ...
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CDKN2B-AS, also known as ANRIL (antisense non-coding RNA in the INK4 locus) is a long non-coding RNA consisting of 19 exons, spanning 126.3kb in the genome, and its spliced product is a 3834bp RNA. It is located within the p15/CDKN2B-p16/CDKN2A-p14/ARF gene cluster, in the antisense direction. Single nucleotide polymorphisms (SNPs) which alter the expression of CDKN2B-AS are associated with many diseases, including coronary artery disease, diabetes and many cancers. It binds to chromobox 7 (CBX7) within the polycomb repressive complex 1 and to SUZ12, a component of polycomb repression complex 2 and through these interactions is involved in transcriptional repression. Long noncoding RNA GRCh38: Ensembl release 89: ENSG00000240498 - Ensembl, May 2017 "Human PubMed Reference:". Cunnington MS, Santibanez Koref M, Mayosi BM, Burn J, Keavney B (2010). Gibson G, ed. "Chromosome 9p21 SNPs Associated with Multiple Disease Phenotypes Correlate with ANRIL Expression". PLoS Genet. 6 (4): e1000899. ...
DB-ID: Database ID of variant, grouping multiple observations of the same variant together, starting with the HGNC gene symbol, followed by an underscore (_) and a six digit number (e.g. DMD_012345). _000000 is used for variants where DNA was not analysed (change predicted from RNA analysis), variants seen in animal models or variants not seen in humans but functionally tested in vitro ...
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CDKN2A; ARF; CDK4I; CDKN2; CMM2; INK4; INK4A; MLM; MTS-1; MTS1; P14; P14ARF; P16; P16-INK4A; P16INK4; P16INK4A; P19; P19ARF; TP16 ...
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Combined effects of increasing numbers of the risk alleles from CDKAL1-rs9465871, CDKN2A/B-rs10811661, IGF2BP2-rs4402960, and SLC30A8-rs13266634. A: The risk al
In 2008, Bilguvar et al22 published their landmark study on the largest GWAS of IA to be published at that time. Their analysis and methods set the stage for future GWAS to build on, and provided additional insight into genomic regions associated with these lesions. The authors used Finnish and Dutch (European) cohorts to comprise the discovery group, which identified candidate SNPs that were subsequently genotyped in 2, pooled Japanese replication cohorts. In total, the study analyzed 2196 cases and 8085 controls. After combining data sets from both groups, SNPs localizing to 3 loci passed the genomic significance threshold. These loci were 2q33.1 (OR, 1.24; P=4.4×10-8), 8q11.23 (OR, 1.36; P=1.4×10−10), and 9p23.1 (OR, 1.29; P=1.4×10−10). These loci are associated with BOLL/PLCL1, SOX17, and CDKN2A-CDKN2B genes, respectively.. In a follow-up study by the same group, Yasuno et al34 added additional cohorts to increase their study population to a monumental 5891 cases and 14181 controls, ...
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An improved thermal ink jet printhead is disclosed for ejecting and propelling ink droplets on demand along a flight path toward a recording medium spaced therefrom in response to receipt of electrical input signals representing digitized data signals. Each printhead has one or more capillary filled ink channels. The channels have a droplet emitting nozzle on one end and connect to an ink supplying manifold on the other end. Each channel has a heating element upstream from the nozzle that is located in a recess. The heating elements are selectively addressable with a current pulse for substantially instantaneous vaporization of the ink contacting the addressed heating element to produce a bubble that expels a droplet of ink during its growth and collapse. The recess walls containing the heating elements prevent the lateral movement of the bubbles through the nozzle and therefore the sudden release of vaporized ink to the atmosphere, known as blowout which causes ingestion of air and interrupts the
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The expression of cyclin-dependent kinase inhibitors p15, p16, p21, and p27 during ovarian follicle growth initiation in the...The expression of cyclin-dependent kinase inhibitors p15, p16, p21, and p27 during ovarian follicle growth initiation in the...

... a cyclin dependent kinase (CDK), and a cyclin dependent kinase inhibitor (CDKI). The progression of cells through the cell ... cyclin-dependent kinases (CDKs), growth suppressor genes and cyclin-dependent kinase inhibitors (CKIs). Oncogene. 1995, 11: 211 ... The expression of cyclin-dependent kinase inhibitors p15, p16, p21, and p27 during ovarian follicle growth initiation in the ... Cyclin-dependent kinase inhibitors (CDKIs) are proteins that bind to and inhibit the activity of CDKs. Two major classes of CDK ...
more infohttps://rbej.biomedcentral.com/articles/10.1186/1477-7827-1-41

Simultaneous Inactivation of the p16, p15 and p14 Genes Encoding Cyclin-Dependent Kinase Inhibitors in Canine T-Lymphoid Tumor...Simultaneous Inactivation of the p16, p15 and p14 Genes Encoding Cyclin-Dependent Kinase Inhibitors in Canine T-Lymphoid Tumor...

Deletion of the p15-p14-p16 genomic locus could be one of the molecular aberrations in canine lymphoid tumor cells. ... Two of the six canine lymphoid tumor cell lines did not express detectable levels of p16, p15 and p14 mRNAs, and wide-ranging ... Based on the sequence data, primers specific for p16, p15 and p14 were designed. Using these primers, the expression of p16, ... p15 and p14 mRNAs could be individually evaluated by reverse transcriptase polymerase chain reaction. Genomic aberrations were ...
more infohttp://altmetrics.ceek.jp/article/www.jstage.jst.go.jp/article/jvms/advpub/0/advpub_12-0351/_article/-char/ja/

Plus itPlus it

1995) Transforming growth factor β activates the promoter of cyclin-dependent kinase inhibitor p15INK4B through an Sp1 ... and TGF-β activates cyclin-dependent kinase inhibitor p15INK4B (Li et al., 1995; Collazo et al., 1992) and α2(I) collagen gene ... two are for cyclin-dependent protein kinase (CDK) (Ser/Thr-ProX-Lys/Arg) (Moodie et al., 1993), and one is for glycogen ... 1993) Complex of ras-GTP with raf1 and mitogen-activated protein kinase kinase. Science 260:1658-1661. ...
more infohttp://www.jneurosci.org/content/17/22/8657

CDKN2B - WikipediaCDKN2B - Wikipedia

"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... "Entrez Gene: CDKN2B cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4)". Rual JF, Venkatesan K, Hao T, Hirozane- ... an alternatively spliced form of p15 cyclin-dependent kinase inhibitor". Cancer Res. 57 (14): 2966-73. PMID 9230210. Rich JN, ... Cyclin-dependent kinase 4 inhibitor B also known as multiple tumor suppressor 2 (MTS-2) or p15INK4b is a protein that is ...
more infohttps://en.wikipedia.org/wiki/CDKN2B

Articles Added on November 17, 2012Articles Added on November 17, 2012

... a cyclin-dependent kinase inhibitor ... ... The expression of p15(INK4b), ... Cytochrome P450 (CYP)-dependent eicosanoids regulate vascular function, inflammation, and angiogenesis, which are ... The outcomes of ecologically more relevant ramping experiments, however, are dependent on the rate of temperature change ... Plaque-Stabilizing Effect of Angiotensin-Converting Enzyme Inhibitor and/or Angiotensin Receptor Blocker in a ... ...
more infohttp://www.biomedsearch.com/added/20121117-p10.html

Cell Division Cycle | www.antibodies-online.comCell Division Cycle | www.antibodies-online.com

This gene encodes a potent cyclin-dependent kinase inhibitor. The encoded protein binds to and inhibits the activity of cyclin- ... Cyclin-Dependent Kinase 5): CDK5 antibodies CDK5 ELISA Kits CDK5 Proteins CDK7 (Cyclin-Dependent Kinase 7): CDK7 antibodies ... Cyclin-Dependent Kinase 8): CDK8 antibodies CDK8 ELISA Kits CDK8 Proteins CDK9 (Cyclin-Dependent Kinase 9): CDK9 antibodies ... Cyclin-Dependent Kinase 3): CDK3 antibodies CDK3 ELISA Kits CDK3 Proteins CDKL3 (Cyclin-Dependent Kinase-Like 3): CDKL3 ...
more infohttps://www.antibodies-online.com/cell-division-cycle-pathway-13/

The CDKN2B gene and its putative association with human ageingThe CDKN2B gene and its putative association with human ageing

P15; MTS2; INK4B; TP15; CDK4I; p15INK4b Common name. cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) Potential ... cyclin-dependent protein serine/threonine kinase inhibitor activity. GO:0005515; protein binding. GO:0019901; protein kinase ... GO:0000079; regulation of cyclin-dependent protein serine/threonine kinase activity. GO:0000086; G2/M transition of mitotic ... The p15 tumor suppressor (CDKN2B) is located in the same region as p16 (CDKN2A), and is also involved in cell cycle, senescence ...
more infohttp://genomics.senescence.info/genes/entry.php?id=0288

The CDKN2B gene and its putative association with human ageingThe CDKN2B gene and its putative association with human ageing

P15; MTS2; INK4B; TP15; CDK4I; p15INK4b Common name. cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) Potential ... cyclin-dependent protein serine/threonine kinase inhibitor activity. GO:0005515; protein binding. GO:0019901; protein kinase ... GO:0000079; regulation of cyclin-dependent protein serine/threonine kinase activity. GO:0000086; G2/M transition of mitotic ... The p15 tumor suppressor (CDKN2B) is located in the same region as p16 (CDKN2A), and is also involved in cell cycle, senescence ...
more infohttp://genomics.senescence.info/genes/entry.php?id=288

GO Gene ListGO Gene List

Cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4). NM_078487. NM_004936. Gene Info. ... Cyclin-dependent kinase inhibitor 1C (p57, Kip2). NM_000076. NM_001122630. NM_001122631. Gene Info. ... Cyclin-dependent kinase inhibitor 2A. NM_001195132. NM_000077. NM_058197. NM_058195. Gene Info. ... Cyclin-dependent kinase 1. NM_001786. NM_001170406. NM_033379. NM_001170407. Gene Info. ...
more infohttps://cgap.nci.nih.gov/Genes/GoGeneQuery?PAGE=1&ORG=Hs&GOID=0023056

GO Gene ListGO Gene List

Cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4). NM_078487. NM_004936. Gene Info. ... Cyclin-dependent kinase inhibitor 1C (p57, Kip2). NM_000076. NM_001122630. NM_001122631. Gene Info. ... Cyclin-dependent kinase inhibitor 2A. NM_001195132. NM_000077. NM_058197. NM_058195. Gene Info. ... Cyclin-dependent kinase 1. NM_001786. NM_001170406. NM_033379. NM_001170407. Gene Info. ...
more infohttps://cgap.nci.nih.gov/Genes/GoGeneQuery?PAGE=1&ORG=Hs&GOID=0010647

CDKN2B Gene - GeneCards | CDN2B Protein | CDN2B AntibodyCDKN2B Gene - GeneCards | CDN2B Protein | CDN2B Antibody

Cyclin Dependent Kinase Inhibitor 2B, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards ... cyclin dependent kinases 4 and 6 (CDK4/CDK6) inhibitor,p15,regulator of cell cycle,passage through the G1 checkpoint,tightly ... Cyclin-dependent kinase 4 inhibitor B Protein Accession:. P42772. Secondary Accessions: *O15125 ... CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) is a Protein Coding gene. Diseases associated with CDKN2B include Scrotal ...
more infohttp://www.genecards.org/cgi-bin/carddisp.pl?gene=CDKN2B&snp=178&rf=/home/genecards/current/website/carddisp.pl

CDKN2B Gene - GeneCards | CDN2B Protein | CDN2B AntibodyCDKN2B Gene - GeneCards | CDN2B Protein | CDN2B Antibody

Cyclin Dependent Kinase Inhibitor 2B, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards ... cyclin dependent kinases 4 and 6 (CDK4/CDK6) inhibitor,p15,regulator of cell cycle,passage through the G1 checkpoint,tightly ... Cyclin-dependent kinase 4 inhibitor B Protein Accession:. P42772. Secondary Accessions: *O15125 ... CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) is a Protein Coding gene. Diseases associated with CDKN2B include Adult Acute ...
more infohttp://www.genecards.org/cgi-bin/carddisp.pl?gene=CDKN2B&rf=/home/genecards/current/website/carddisp.pl&bioalma_dis=86

HCV and Oxidative Stress: Implications for HCV Life Cycle and HCV-Associated PathogenesisHCV and Oxidative Stress: Implications for HCV Life Cycle and HCV-Associated Pathogenesis

An upregulation of the cyclin-dependent kinase inhibitor p15 and of the proapoptotic protein Bim can be observed. There is ... Based on a screen of various kinase inhibitors, p38MAPK and Janus kinase were identified to mediate Nrf2 phosphorylation/ ... ARE-dependent genes are involved in the removal of ROI, that is, glutathione-dependent peroxidase (GPx), in the glutathione ... AMP-activated protein kinase inhibits the mTOR kinase activity, causing an activation of autophagy [105]. This canonical ...
more infohttps://www.hindawi.com/journals/omcl/2016/9012580/

adenocarcinoma in situ of lung diagnosis 2005:2010[pubdate] *count=100 - BioMedLib™ search engineadenocarcinoma in situ of lung diagnosis 2005:2010[pubdate] *count=100 - BioMedLib™ search engine

Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Death-Associated Protein ... Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / H-cadherin; 0 / Insulin-Like Growth ... Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 6.3.2.- / BRAP protein, human ... Calcium-Calmodulin-Dependent Protein Kinases / genetics. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / secondary. ...
more infohttp://www.bmlsearch.com/?kwr=adenocarcinoma+in+situ+of+lung+diagnosis+2005:2010%5Bpubdate%5D&cxts=100&stmp=b0

Atlas StatusAtlas Status

CDKN2B (cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4)). CREATED 2011-01 Lab Cell Oncology, National Cancer ... MAPKAPK2 (mitogen-activated protein kinase-activated protein kinase 2). CREATED 2010-04 Laboratory of Cancer Molecular Biology ... VRK2 (vaccinia related kinase 2). CREATED 2012-05 Instituto de Biologia Molecular y Celular del Cancer, CSIC-Universidad de ... KSR1 (kinase suppressor of ras 1). CREATED 2011-02 Eppley Institute for Cancer Research, University of Nebraska Medical Center ...
more infohttp://atlasgeneticsoncology.org/Status/Status_Auth_F.html

anti-p15 INK4b antibody [DCS-114]  | GeneTexanti-p15 INK4b antibody [DCS-114] | GeneTex

... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4)) for ICC/IF, IP. Anti-p15 INK4b mAb (GTX72279) is tested in Human ... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4). Background. p15INK4b is a specific inhibitor of cdk4/cdk6 and is ... Storage Conditions: p15 INK4b antibody [DCS-114]. Storage Buffer. 10mM Phosphate-buffered saline containing 0.2% BSA and 0.1% ... For IF: Use at an assay dependent dilution. For IP: (Native verified) Use Protein G. Use at a dilution of 1:400. Not suitable ...
more infohttp://www.genetex.com/INK4b-antibody-DCS-114-GTX72279.html

adult acute non lymphocytic leukemia in remission 2005:2010[pubdate] *count=100 - BioMedLib™ search engineadult acute non lymphocytic leukemia in remission 2005:2010[pubdate] *count=100 - BioMedLib™ search engine

Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p57; 0 / DNA-Binding ... Protein Kinase Inhibitors / adverse effects. Pyrimidines / adverse effects. Thiazoles / adverse effects. *[MeSH-minor] Adult. ... The optimal treatment of Philadelphia chromosome-positive patients requires the addition of BCR-ABL tyrosine kinase inhibitors ... Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib ...
more infohttp://www.bmlsearch.com/?kwr=adult+acute+non+lymphocytic+leukemia+in+remission+2005:2010%5Bpubdate%5D&cxts=100&stmp=b0

CDKN2B - PrimePCR Assay and Template | Life Science | Bio-RadCDKN2B - PrimePCR Assay and Template | Life Science | Bio-Rad

cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) Assay Type: Probe Assay Design: exonic Application: Gene Expression ... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) Assay Type: SYBR® Green Assay Design: Exonic Application: Gene ... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) Assay Type: SYBR® Green Assay Design: exonic Application: Gene ... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) Assay Type: EvaGreen Application: Gene Expression Unique Assay ID: ...
more infohttp://www.bio-rad.com/en-us/prime-pcr-assays/gene/cdkn2b-human

CDKN2B monoclonal antibody, clone DCS114 - (MAB2030) - Products - AbnovaCDKN2B monoclonal antibody, clone DCS114 - (MAB2030) - Products - Abnova

CDK4I,INK4B,MTS2,P15,TP15,p15INK4b. *Gene Description:. *cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) ... cyclin-dependent kinase 4 inhibitor B,cyclin-dependent kinase inhibitor 2B,cyclin-dependent kinases 4 and 6 binding protein, ... Inhibitors of mammalian G1 cyclin-dependent kinases.. Sherr CJ, Roberts JM.Genes Dev. 1995 May 15;9(10):1149-63. ... This gene encodes a cyclin-dependent kinase inhibitor, which forms a complex with CDK4 or CDK6, and prevents the activation of ...
more infohttps://www.abnova.com/products/products_detail.asp?Catalog_id=MAB2030

CBFα3 (AML2) Is Induced by TGF-β1 to Bind and Activate the Mouse Germline Ig α Promoter | The Journal of ImmunologyCBFα3 (AML2) Is Induced by TGF-β1 to Bind and Activate the Mouse Germline Ig α Promoter | The Journal of Immunology

Transforming growth factor β activates the promoter of cyclin-dependent kinase inhibitor P15INK4B through a Sp1 consensus site ... Bach2 Promotes B Cell Receptor-Induced Proliferation of B Lymphocytes and Represses Cyclin-Dependent Kinase Inhibitors ... Identification of regulatory sequences in the type I plasminogen activator inhibitor gene responsive to TGFβ. J. Biol. Chem. ... Assembly and function of a TCRα enhancer complex is dependent on LEF-1-induced DNA bending and multiple protein-protein ...
more infohttp://www.jimmunol.org/content/161/12/6751

Demethylation of a hypermethylated P15/INK4B gene in patients with myelodysplastic syndrome by 5-Aza-2′-deoxycytidine ...Demethylation of a hypermethylated P15/INK4B gene in patients with myelodysplastic syndrome by 5-Aza-2′-deoxycytidine ...

p15, a target of transforming growth factor-β signaling,16 is an inhibitor of the cyclin-dependent kinase-417 18 and a negative ... p16 and p15, 2 inhibitors of cyclin-dependent kinases, are frequently hypermethylated in hematologic neoplasias. Decitabine, or ... Review of alterations of cyclin-dependent kinase inhibitor INK4 family genes p15, p16, p18 and p19 in human leukemia-lymphoma ... Inactivation of the cyclin-dependent kinase inhibitor p15INK4b by deletion and de novo methylation with independence of ...
more infohttp://www.bloodjournal.org/content/100/8/2957?ijkey=0dd972d0b75c32e0a0737436ef03a3e2355508cb&keytype2=tf_ipsecsha&sso-checked=true

June | 2019 | Regulation of human neutrophil-mediated cartilage proteoglycan degradationJune | 2019 | Regulation of human neutrophil-mediated cartilage proteoglycan degradation

Nanjing, China). Primary antibodies against Cyclin-dependent kinase inhibitor 2B (P15) (cat. no. AB33457), Cyclin D1 (cat. no. ... although it collaborates with p53 to modify cyclin G2 appearance. Furthermore, this pathway regulates and cyclin G2 through ... Primers were labeled with 32P-ATP using T4 kinase. After the labeling reaction, the mixtures were cleared with G-50 minicolumns ... Cellular DNA was stained with propidium iodide (Nanjing KeyGen Biotech Co., Ltd.). Cell routine distributions were dependant on ...
more infohttp://acmbcb.org/2019/06/

Concurrent disruption of p16 INK4a and the ARF-p53 pathway predicts poor prognosis in aggressive non-Hodgkins lymphoma |...Concurrent disruption of p16 INK4a and the ARF-p53 pathway predicts poor prognosis in aggressive non-Hodgkin's lymphoma |...

Koduru PR, Zariwala M, Soni M, Gong JZ, Xiong Y, Broome JD . Deletion of cyclin-dependent kinase 4 inhibitor genes P15 and P16 ... including the gene encoding the cyclin-dependent kinase inhibitor p15INK4b, the interferon gene cluster, and the ... Gombart AF, Morosetti R, Miller CW, Said JW, Koeffler HP . Deletions of the cyclin-dependent kinase inhibitor genes p16INK4A ... The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases Cell 1993 75: 805-816 ...
more infohttps://www.nature.com/articles/2401901?error=cookies_not_supported&code=c5ce3218-c86c-42fa-9fbc-b24ddb0994e9

Cyclin-dependent kinase 4 - WikipediaCyclin-dependent kinase 4 - Wikipedia

"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... See also CDK inhibitor for inhibitors of various CDKs. Cyclin-dependent kinase 4 has been shown to interact with: CDC37, CDKN1B ... 1995). "Identification of human cyclin-dependent kinase 8, a putative protein kinase partner for cyclin C". Proc. Natl. Acad. ... "The nuclear protein p34SEI-1 regulates the kinase activity of cyclin-dependent kinase 4 in a concentration-dependent manner". ...
more infohttps://en.wikipedia.org/wiki/Cyclin-dependent_kinase_4

RPRD1A Full-Length MS Protein Standard - Creative ProteomicsRPRD1A Full-Length MS Protein Standard - Creative Proteomics

P15RS is upregulated in cells overexpressing cyclin-dependent kinase inhibitor p15(INK4b) (CDKN2B; MIM 600431) and may have a ... P15RS is upregulated in cells overexpressing cyclin-dependent kinase inhibitor p15(INK4b) (CDKN2B; MIM 600431) and may have a ...
more infohttps://www.creative-proteomics.com/product/detail-cpfl312551_4850.htm
  • We examined p15 and p16 methylation status in bone marrow mononuclear cells from patients with high-risk MDS during treatment with decitabine, using a methylation-sensitive primer extension assay (Ms-SNuPE) to quantitate methylation, and denaturing gradient gel electrophoresis (DGGE) and bisulfite-DNA sequencing to distinguish individually methylated alleles. (bloodjournal.org)
  • Methylation-specific PCR was used to determine the methylation status of p16, p15 , and ras association domain family 1A ( RASSF1A ). (aacrjournals.org)
  • Also phosphorylates SMAD3 in a cell-cycle-dependent manner and represses its transcriptional activity. (wikipedia.org)
  • Unlike in solid tumors, the 5′ region of p15 but not p16 is frequently methylated in AML 5 7 and MDS. (bloodjournal.org)
  • Thus, these authors suggested that inability to up-regulate p15 and p16 would promote cellular proliferation and atherosclerosis. (onlinejacc.org)
  • 19 p15 is highly homologous to and colocalized with p16 within a ∼25-kb region on the short arm of human chromosome 9. (bloodjournal.org)
  • Based on the sequence data, primers specific for p16, p15 and p14 were designed. (ceek.jp)
  • The emergence of partially demethylated epigenotypes and re-establishment of normal p15 protein expression following the initial decitabine courses implicate pharmacologic demethylation as a possible mechanism resulting in hematologic response in MDS. (bloodjournal.org)