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 E: A 50-kDa protein that complexes with CYCLIN-DEPENDENT KINASE 2 in the late G1 phase of the cell cycle.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-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.Cell Proliferation: All of the processes involved in increasing CELL NUMBER including CELL DIVISION.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.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.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 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 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.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.Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.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.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-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.Cyclin D3: A broadly expressed type D cyclin. Experiments using KNOCKOUT MICE suggest a role for cyclin D3 in LYMPHOCYTE development.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Retinoblastoma Protein: Product of the retinoblastoma tumor suppressor gene. It is a nuclear phosphoprotein hypothesized to normally act as an inhibitor of cell proliferation. Rb protein is absent in retinoblastoma cell lines. It also has been shown to form complexes with the adenovirus E1A protein, the SV40 T antigen, and the human papilloma virus E7 protein.Cell Division: The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.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.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.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.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.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.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.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.Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein.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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.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.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.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.G2 Phase: The period of the CELL CYCLE following DNA synthesis (S PHASE) and preceding M PHASE (cell division phase). The CHROMOSOMES are tetraploid in this point.Cyclin G: A cyclin subtype that is found associated with CYCLIN-DEPENDENT KINASE 5; cyclin G associated kinase, and PROTEIN PHOSPHATASE 2.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.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.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.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.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.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.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.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.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.Antineoplastic Agents: Substances that inhibit or prevent the proliferation of NEOPLASMS.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)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.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.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.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.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.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.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.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.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.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.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.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.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.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.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)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.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).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.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.Kinetics: The rate dynamics in chemical or physical systems.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.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.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.Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.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.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.Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.HeLa Cells: The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.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.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Benzamides: BENZOIC ACID amides.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.Mice, Inbred C57BLProtein Structure, Tertiary: The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.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.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.Cyclin T: A cyclin subtype that is found associated with CYCLIN-DEPENDENT KINASE 9. Unlike traditional cyclins, which regulate the CELL CYCLE, type T cyclins appear to regulate transcription and are components of positive transcriptional elongation factor B.Cyclin H: A cyclin subtype that is found as a component of a heterotrimeric complex containing cyclin-dependent kinase 7 and CDK-activating kinase assembly factor. The complex plays a role in cellular proliferation by phosphorylating several CYCLIN DEPENDENT KINASES at specific regulatory threonine sites.Flavonoids: A group of phenyl benzopyrans named for having structures like FLAVONES.DNA Primers: Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.Chromones

*P16

"Entrez Gene: CDKN2A cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4)". Nobori T, Miura K, Wu DJ, Lois A, ... p16 acts as a tumor suppressor by binding to CDK4/6 and preventing its interaction with cyclin D. This interaction ultimately ... p16 is also known as: p16Ink4A p16Ink4 Cyclin-dependent kinase inhibitor 2A (CDKN2A) CDKN2 CDK 4 Inhibitor Multiple Tumor ... p16 is a cyclin-dependent kinase (CDK) inhibitor that slows down the cell cycle by prohibiting progression from G1 phase to S ...

*Cyclin D

... activate cyclin D gene in response to integrin. p27kip1 and p21cip1 are cyclin-dependent kinase inhibitors (CKIs) which ... P16 functions in inactivating cyclin D/Cdk 4 complex. Thus, blocking transcription of INK4 gene would increase cyclin D/Cdk4 ... Hence, INK4 binds to cyclin D- dependent CDKs and inactivates the whole complex. Glycogen synthase kinase three beta, GSK3β, ... Inactivation of cyclin D is triggered by several cyclin-dependent kinase inhibitor protein (CKIs) like the INK4 family (e.g. ...

*CDKN2B

"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... This gene encodes a cyclin-dependent kinase inhibitor, also known as p15Ink4b protein, which forms a complex with CDK4 or CDK6 ... "Entrez Gene: CDKN2B cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4)". Rual JF, Venkatesan K, Hao T, Hirozane- ... 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 6

"Both p16 and p21 families of cyclin-dependent kinase (CDK) inhibitors block the phosphorylation of cyclin-dependent kinases by ... The protein encoded by this gene is a member of the cyclin-dependent kinase, (CDK) family, which includes CDK4. CDK family ... "Crystal structure of the complex of the cyclin D-dependent kinase Cdk6 bound to the cell-cycle inhibitor p19INK4d". Nature. 395 ... A Cyclin-dependent kinase 6 interacts with: CDKN2C, Cyclin D1, Cyclin D3, P16, PPM1B, and PPP2CA. Cell cycle, Mitosis, CDK, ...

*CDKN2A

"Transcriptional repression of the D-type cyclin-dependent kinase inhibitor p16 by the retinoblastoma susceptibility gene ... When working normally, p16 binds to the cyclic dependent kinases CDK4 to inhibit their ability to create tumors, but when ... p16 inhibits cyclin dependent kinases 4 and 6 (CDK4 and CDK6) and thereby activates the retinoblastoma (Rb) family of proteins ... "CDKN2A cyclin dependent kinase inhibitor 2A [Homo sapiens (human)] - Gene - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2016-10-11. ...

*CDKN2D

"Entrez Gene: CDKN2D cyclin-dependent kinase inhibitor 2D (p19, inhibits CDK4)". Hirai H, Roussel MF, Kato JY, et al. (1995). " ... 1998). "Crystal structure of the complex of the cyclin D-dependent kinase Cdk6 bound to the cell-cycle inhibitor p19INK4d". ... 2004). "Antitumour effect of cyclin-dependent kinase inhibitors (p16(INK4A), p18(INK4C), p19(INK4D), p21(WAF1/CIP1) and p27( ... Cyclin-dependent kinase 4 inhibitor D is an enzyme that in humans is encoded by the CDKN2D gene. The protein encoded by this ...

*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 ... Cyclin-dependent kinase 4 also known as cell division protein kinase 4 is an enzyme that in humans is encoded by the CDK4 gene ... Kato JY, Matsuoka M, Strom DK, Sherr CJ (1994). "Regulation of cyclin D-dependent kinase 4 (cdk4) by cdk4-activating kinase". ... "Direct binding of cyclin D to the retinoblastoma gene product (pRb) and pRb phosphorylation by the cyclin D-dependent kinase ...

*Cyclin D1

"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... Cyclin D1 is a regulatory subunit of cyclin-dependent kinases CDK4 and CDK6. The protein dimerizes with CDK4/6 to regulate the ... Cyclin-D1 is a protein that in humans is encoded by the CCND1 gene. The CCND1 gene encodes the cyclin D1 protein. The human ... binding motif; cyclin box domain for cyclin-dependent kinase (CDK) binding and CDK inhibitor binding; LxxLL binding motif for ...

*Cell cycle checkpoint

p16 disrupts cyclin D-CDK4 complexes, thus causing the release of p21 from the complexes, which leads to the dephosphorylation ... checkpoints is through the regulation of the activities of a family of protein kinases known as the cyclin-dependent kinases ( ... CDKs), which bind to different classes of regulator proteins known as cyclins, with specific cyclin-CDK complexes being formed ... an inhibitor of the G1-to-S promoting complex cyclin E-CDK2. In addition, another mechanism by which p21 is activated is ...

*CDKN2C

"Entrez Gene: CDKN2C cyclin-dependent kinase inhibitor 2C (p18, inhibits CDK4)". Ewing RM, Chu P, Elisma F, Li H, Taylor P, ... "Antitumour effect of cyclin-dependent kinase inhibitors (p16(INK4A), p18(INK4C), p19(INK4D), p21(WAF1/CIP1) and p27(KIP1)) on ... "Identification of functional elements of p18INK4C essential for binding and inhibition of cyclin-dependent kinase (CDK) 4 and ... CDKN2C has been shown to interact with Cyclin-dependent kinase 4 and Cyclin-dependent kinase 6. GRCh38: Ensembl release 89: ...

*Retinoblastoma protein

... cyclin E and cyclin A), which push the cell through the cell cycle by activating cyclin-dependent kinases, and a molecule ... Furthermore, triple knockout, p16 addition, and Cdk 4/6 inhibitor addition experiments as confirmed that Cyclin D- Cdk 4/6 is ... "The retinoblastoma-susceptibility gene product binds directly to the human TATA-binding protein-associated factor TAFII250". ... To further add to this point, the HDAC-Rb complex is shown to be disrupted by cyclin D/Cdk4 which levels increase and peak ...

*Epithelioid sarcoma

Cyclin D-1 is a regulator of cyclin-dependent kinases (CDK4 and CDK6). It has been shown to interact with the retinoblastoma ... Tyrosine kinase Inhibitors block the action of these enzymes. Tyrosine kinase inhibitors have been shown to inhibit the VEGF, ... "Epithelioid sarcoma expresses epidermal growth factor receptor but gene amplification and kinase domain mutations are rare". ... Upon ligand binding, EGFR phosphorylation triggers the activation of downstream signaling pathways involved in critical ...

*TP53

"Characterization of cells and gene-targeted mice deficient for the p53-binding kinase homeodomain-interacting protein kinase 1 ... "p53 is phosphorylated by CDK7-cyclin H in a p36MAT1-dependent manner". Molecular and Cellular Biology. 17 (12): 7220-9. doi: ... p21 (WAF1) binds to the G1-S/CDK (CDK4/CDK6, CDK2, and CDK1) complexes (molecules important for the G1/S transition in the cell ... P16, PARC, PARP1, PIAS1, CDC14B, PIN1, PLAGL1, PLK3, PRKRA, PHB, PML, PSME3, PTEN, PTK2, PTTG1, RAD51, RCHY1, RELA, Reprimo ...
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.
Opens the Highlight Feature Bar and highlights feature annotations from the FEATURES table of the record. The Highlight Feature Bar can be used to navigate to and highlight other features and provides links to display the highlighted region separately. Links in the FEATURES table will also highlight the corresponding region of the sequence. More... ...
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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 ...
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 ...
Looking for online definition of cyclin-dependent kinase 15 in the Medical Dictionary? cyclin-dependent kinase 15 explanation free. What is cyclin-dependent kinase 15? Meaning of cyclin-dependent kinase 15 medical term. What does cyclin-dependent kinase 15 mean?
TBX3, a member of the T-box family of transcription factors, is essential in development and has emerged as an important player in the oncogenic process. TBX3 is overexpressed in several cancers and has been shown to contribute directly to tumour formation, migration and invasion. However, little is known about the molecular basis for its role in development and oncogenesis because there is a paucity of information regarding its target genes. The cyclin-dependent kinase inhibitor p21WAF1 plays a pivotal role in a myriad of processes including cell cycle arrest, senescence and apoptosis and here we provide a detailed mechanism to show that it ...
Although the androgen receptor (AR) has been implicated in the promotion of apoptosis in testicular cells (TSCs), the molecular pathway underlying AR-mediated apoptosis and its sensitivity to environmental hormones in TSCs and induced pluripotent stem cells (iPSCs) remain unclear. We generated the iPSCs from bovine TSCs via the electroporation of OCT4. The established iPSCs were supplemented with leukemia inhibitory factor and bone morphogenetic protein 4 to maintain and stabilize the expression of stemness genes and their pluripotency. Apoptosis signaling ...
cGMP Dependent Kinase Inhibitor Peptide chemical properties, What are the chemical properties of cGMP Dependent Kinase Inhibitor Peptide 82801-73-8, What are the physical properties of cGMP Dependent Kinase Inhibitor Peptide ect.
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.
MicroRNA-200b and microRNA-200c (miR-200b/c) are 2 of the most frequently upregulated oncomiRs in intestines cancer cells. cell lines. Additionally, we confirmed that dominance of RECK by miR-200b/c therefore brought about SKP2 (S-phase kinase-associated proteins 2) level and g27Kip1 (also known as cyclin-dependent kinase inhibitor 1B) destruction in intestines cancers cells, which promotes cancer cell proliferation […]. Read More ». ...
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
TGF-? is the founding member of a multifunctional family of cytokines that regulate many aspects of cell physiology, including cell growth, differentiation, motility and death and play important roles in many developmental and pathological processes. TGF-? signals by binding to a heterotetrameric complex of type I and type II serine/threonine kinase receptors. The type I receptor is phosphorylated and activated by the type II receptor and propagates the signal to the nucleus by phosphorylating and activating receptor-regulated Smad proteins (R-Smads). Once activated, the R-Smads translocate to the nucleus ...
In this paper, we report that (+)-preussin, a pyrrolidinol alkaloid originally identified as an antifungal agent, has growth-inhibitory and cytotoxic effects on human cancer cells. Preussin was found to be a potent inhibitor of cyclin E kinase (CDK2-cyclin E) in vitro (50% inhibitory concentration; approximately 500 nM) and to inhibit cell cycle progression into S phase. In agreement with these findings, the level of the cyclin-dependent kinase inhibitor p27(KIP-1) is increased in response to preussin treatment while the expression of both ...
Cutaneous T cell lymphomas (CTCLs) represent a heterogeneous group of non-Hodgkin lymphomas that affect the skin. The pathogenesis of these conditions is poorly understood. For example, the signaling mechanisms contributing to the dysregulated growth of the neoplastic T cells are not well defined. Here, we demonstrate that loss of nuclear localization of pro-IL-16 facilitates CTCL cell proliferation by causing a decrease in expression of the cyclin dependent-kinase inhibitor p27Kip1. The decrease in p27Kip1 expression was directly attributable to an increase in expression of S-phase ...
Sustained activation of extracellular signal-regulated kinase (ERK) has been detected previously in numerous tumors in the absence of RAS-activating mutations. However, the molecular mechanisms responsible for ERK-unrestrained activity independent of RAS mutations remain unknown. Here, we evaluated the effects of the functional interactions of ERK proteins with dual-specificity phosphatase 1 (DUSP1), a specific inhibitor of ERK, and S-phase kinase-associated protein 2 (SKP2)/CDC28 protein kinase 1b (CKS1) ubiquitin ligase complex in human hepatocellular carcinoma (HCC). Levels of DUSP1, as assessed by real-time reverse ...
Although the induction of senescence in cancer cells is a potent mechanism of tumor suppression, senescent cells remain metabolically active and may secrete a broad spectrum of factors that promote tumorigenicity in neighboring malignant cells. Here we show that androgen deprivation therapy (ADT), a widely used treatment for advanced prostate cancer, induces a senescence-associated secretory phenotype in prostate cancer epithelial cells, indicated by increases in senescence-associated beta-galactosidase activity, heterochromatin protein 1 beta foci, and expression of cathepsin B and insulin-like growth factor binding protein 3. Interestingly, ADT also induced high levels of vimentin expression in prostate ...
Plant S-phase kinase-associated protein 1 (SKP1) genes play crucial roles in plant development and differentiation. However, the role of SKP1 in citrus is unclear. Herein, we described a novel SKP1-like gene, designated as CrWSKP1, from
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The human cyclin-dependent kinase inhibitor 2A (CDKN2A) gene generates several transcript variants that differ in their first exons. At least three alternatively spliced variants encoding distinct proteins have been reported. One of these, cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4) or p16INK4a, interacts with, and sequesters, the E3 ubiquitin-protein ligase MDM2, a protein responsible for the degradation of p53. Thus, p16-INK4a functions as a tumor suppressor in a variety of cells. Mutations in the CDKN2A ...
Background Over the last decade a number of species, from farm animals to rodents, have been cloned using somatic cell nuclear transfer technology (SCNT). This technique has the potential to revolutionize the way that genetically modified animals are made. In its current state, the process of SCNT is very inefficient (|5% success rate), with several technical and biological hurdles hindering development. Yet, SCNT provides investigators with powerful advantages over other approaches, such as allowing for prescreening for the desired level of transgene expression and eliminating the excess production of undesirable wild-type animals. The rat plays a significant role in biomedical research, but SCNT has been problematic for this ...
Largely on the basis of studies using the potent clastogen ionizing radiation, it has been widely assumed that up-regulation of the cyclin-dependent kinase inhibitor p21waf1cip1 in cultured cells exposed to DNA-damaging agents is contingent upon the presence of functional p53 tumor suppressor protein. Nevertheless, we demonstrate here that the model mutagen 254-nm UV light induces p21waf1cip1 protein and concomitant G1 arrest in normal human skin fibroblasts, as well as in p53-deficient fibroblasts derived from cancer-prone Li-Fraumeni syndrome patients. However, as expected, following exposure to ionizing ...
MicroRNAs (miRNA) have tumor suppressive and oncogenic potential in human cancer, but whether and how miRNAs control cell cycle progression is not understood. To address this question, we carried out a comprehensive analysis of miRNA expression during serum stimulation of quiescent human cells. Time course analyses revealed that four miRNAs are up-regulated and |100 miRNAs are down-regulated, as cells progress beyond the G(1)-S phase transition. We analyzed the function of two up-regulated miRNAs (miR-221 and miR-222) that are both predicted to target the cell growth suppressive cyclin-dependent kinase inhibitors p27 and p57. Our results show that miR-221 and miR-222 both ...
Looking for online definition of Cell cycle regulatory protein in the Medical Dictionary? Cell cycle regulatory protein explanation free. What is Cell cycle regulatory protein? Meaning of Cell cycle regulatory protein medical term. What does Cell cycle regulatory protein mean?
Activation of growth factor receptors by ligand binding initiates a cascade of events leading to cell growth and division. Progression through the cell cycle is controlled by cyclin-dependent protein kinases (Cdks), but the mechanisms that link growth factor signaling to the cell cycle machinery have not been established. We report here that Ras proteins play a key role in integrating mitogenic signals with cell cycle progression through G1. Ras is required for cell cycle progression and activation of both Cdk2 and Cdk4 until approximately 2 h before the G1/S transition, corresponding to the restriction point. Analysis of Cdk-cyclin ...
Supinoxin, also known as RX-5902, is orally bioavailable small molecule inhibitor of phosphorylated-p68 RNA helicase (P-p68), with potential anti-proliferative and antineoplastic activity. Upon oral administration, P-p68 inhibitor RX-5902 may both inhibit the activity of the anti-apoptotic B-cell lymphoma 2 (Bcl-2) protein and facilitate the induction of cyclin-dependent kinase inhibitor 1 (p21). This may prevent G2/M cell cycle progression and lead to growth inhibition in tumor cells. P-p68 is overexpressed in various ...
The non-receptor-type tyrosine kinase c-Abl functions as a cytoplasmic signal transducer upon activation of cell-surface receptors. c-Abl is also involved in DDR (DNA-damage response), which is initiated in the nucleus, whereas its molecular functions in DDR are not fully understood. In the present study, we found that c-Abl phosphorylates JunB, a member of the AP-1 (activator protein 1) transcription factor family. Because JunB was suggested to be involved in DDR, we analysed the role of c-Abl-mediated phosphorylation of JunB in DDR. We first analysed phosphorylation sites of JunB and found that c-Abl majorly phosphorylates JunB at Tyr173, Tyr182 and Tyr188. Because c-Abl ...
ECM accumulation and ASMC proliferation are hallmarks in the development of intimal thickenings associated with the development of atherosclerotic lesions.61 Our recent work has shown that insertion of decorin-overexpressing cells into injured arteries causes a decrease in intimal volume.30 This decrease is due primarily to a decrease in ECM volume rather than a change in cell number within the intima. The results of the present in vitro study support these in vivo observations and, furthermore, suggest that the effects of decorin overexpression may involve the modulation of TGF-β activity.. An initial decrease in DNA synthesis by decorin-overexpressing cells was observed during the first 24 hours after plating, but this relative decrease disappeared at later time points. ...
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 ...
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.
Objective: Breast cancer is global female health problem worldwide. Most of the currently used agents for breast cancer treatment have toxic side-effects. Ginseng root, an oriental medicine, has many health benefits and may exhibit direct anti-cancer properties. This study was performed to assess the effects of ginseng on breast cancer cell lines. Materials and Methods: Cytotoxicity of ginseng extract was measured by MTT assay after exposure of MDA-MB-231, MCF-10A and MCF-7 breast cancer cells to concentrations of 0.25, 0.5, 1, 1.5, 2 and 2.5 mg/well. Expression levels of p21WAF, p16INK4A, Bcl-2, Bax and P53 genes were analyzed by quantitative real time PCR. Results: The treatment resulted in inhibition of cell proliferation in a dose-and time-dependent manner. ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Genetic variation at the chromosome 9p21 risk locus promotes cardiovascular disease; however, it is unclear how or which proteins encoded at this locus contribute to disease. We have previously demonstrated that loss of one candidate gene at this locus, cyclin-dependent kinase inhibitor 2B (Cdkn2b), in mice promotes vascular SMC apoptosis and aneurysm progression. Here, we investigated the role of Cdnk2b in atherogenesis and found that in a mouse model of atherosclerosis, deletion of Cdnk2b promoted advanced development of atherosclerotic plaques composed of large necrotic cores. Furthermore, human carriers of the 9p21 risk allele had ...
The KOMP Repository Collection is located at the MMRRC at the University of California, Davis and Childrens Hospital Oakland Research Institute. Question? Comments? For Mice, Cells, and germplasm please contact us at [email protected], US 1-888-KOMP-MICE or International +1-530-752-KOMP, or for vectors komp[email protected] or +1-510-450-7917 ...
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 ...
... cellular proliferation via inhibition of CDK activities. routine and g27Kip1 (hereafter g27) can regulate CDK actions.1-3 The p27 protein was originally known as an inhibitor of CDK activities for things containing CDK2 and shown to inhibit cyclin E and cyclin A activities which regulate G1 and S phase traverse.4-6 In addition to CDK inhibition, g27 provides other multifarious connections with cyclin N/cdk4 processes putatively.7 Since cellular amounts of g27 are elevated in response to high cell thickness, serum deprival, and TGF, it was hypothesized g27 brought cells into quiescence and held them in G0 through the inhibition of CDK ...
Recombinant Cyclin-Dependent Kinase 10 (CDK10) Protein (His tag). Species: Cow (Bovine). Source: Yeast. Order product ABIN1616360.
Recombinant Cyclin-Dependent Kinase 10 (CDK10) Protein (His tag). Species: Human. Source: Insect Cells. Order product ABIN3091398.
Complete information for CDKN2B gene (Protein Coding), Cyclin Dependent Kinase Inhibitor 2B, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Complete information for CDKN2B gene (Protein Coding), Cyclin Dependent Kinase Inhibitor 2B, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
2vtp: Identification of N-(4-piperidinyl)-4-(2,6-dichlorobenzoylamino)-1H-pyrazole-3-carboxamide (AT7519), a novel cyclin dependent kinase inhibitor using fragment-based X-ray crystallography and structure based drug design.
Clone REA756 recognizes the human CD20L, an intracytoplasmic membrane protein, which is also known as Htm4 or MS4A3. It is present specifically in hematopoietic cells and tissues. CD20L functions as a hematopoietic modulator for the G1-S cell cycle transition. It binds to cyclin-dependent kinase inhibitor 3 (CDKN3/KAP) and modulates the level of phosphorylation of cyclin-dependent kinase 2 (CDK2). Additional information: Clone REA756 displays negligible binding to Fc receptors. - Österreich
TY - JOUR. T1 - Dinaciclib induces anaphase catastrophe in lung cancer cells via inhibition of cyclin-dependent kinases 1 and 2. AU - Danilov, Alexey. AU - Hu, Shanhu. AU - Orr, Bernardo. AU - Godek, Kristina. AU - Mustachio, Lisa Maria. AU - Sekula, David. AU - Liu, Xi. AU - Kawakami, Masanori. AU - Johnson, Faye M.. AU - Compton, Duane A.. AU - Freemantle, Sarah J.. AU - Dmitrovsky, Ethan. PY - 2016/11/1. Y1 - 2016/11/1. N2 - Despite advances in targeted therapy, lung cancer remains the most common cause of cancer-related mortality in the United States. Chromosomal instability is a prominent feature in lung cancer and, because it rarely occurs in normal cells, it represents a potential therapeutic target. Our prior work discovered that lung cancer cells ...
We have previously shown that Nodal and ALK7 are expressed in human placenta (Roberts et al., 2003) and that Nodal signalling through ALK7 inhibits trophoblast cell proliferation (Munir et al., 2004), migration and invasion (Nadeem et al., 2011). In this study, we provided evidence that p27 is a key mediator of Nodal signalling in trophoblast cells. We found that Nodal not only upregulated p27 expression, but also induced p27 and CDK2 translocation to the cytoplasm, leading to inhibition of cell proliferation and migration/invasion.. The present study demonstrates that Nodal upregulates p27 mRNA and protein levels through multiple mechanisms. First, we found that in the ...
Alterations in proliferation and hypertrophy of renal mesangial cells are typical features of diabetic nephropathy. The HP (hexosamine pathway) has been proposed as a biochemical hypothesis to explain microvascular alterations due to diabetic nephropathy; however, involvement of HP in the regulation of mesangial cell growth or hypertrophy has been poorly studied. Although gangliosides are known to regulate cell proliferation, their potential role in mesangial cell-growth perturbations has hardly been explored. In the present study, we investigated the effects of the HP activation, mimicked by GlcN ...
TBX3, a member of the T-box family of transcription factors, is essential in development and has emerged as an important player in the oncogenic process. TBX3 is overexpressed in several cancers and has been shown to contribute directly to tumour formation, migration and invasion. However, little is known about the molecular basis for its role in development and oncogenesis because there is a paucity of information regarding its target genes. The cyclin-dependent kinase inhibitor p21WAF1 plays a pivotal role in a myriad of processes including cell cycle arrest, senescence and apoptosis and here we provide a detailed mechanism to show that it ...
The protein encoded by WT1 belongs to a class of zinc-binding transcription factors, with multiple variants produced by alternative splicing. The four zinc-finger domains of WT1 recognize GC-rich DNA target sequences, an effect that is modulated by the variable insertion of three amino acids (KTS) between zinc fingers 3 and 4. WT1 appears to function as a transcriptional repressor, although physiologically relevant target genes remain to be defined. Potential protein interactors include another tumor suppressor gene product, p53, whose function is modulated by WT1. Inducible expression of WT1 in tissue culture cells triggers apoptosis, associated with ...
Studies suggest that Hsf4 expression correlates with its role in cell growth and differentiation. However, the role of Hsf4 in tumorigenesis in vivo remains unexplored. In this article, we provide evidence that absence of the Hsf4 gene suppresses evolution of spontaneous tumors arising in p53- or Arf-deficient mice. Furthermore, deletion of hsf4 alters the tumor spectrum by significantly inhibiting development of lymphomas that are normally observed in the majority of mice lacking p53 or Arf tumor suppressor genes. Using mouse embryo fibroblasts deficient in the hsf4 gene, we have found that these cells exhibit reduced proliferation that is associated with induction of senescence and senescence-associated ...
The Notch family of transmembrane receptors regulates both cell fate decisions and the maintenance of adult stem cells, processes that require precise control of the cell cycle. Although Notch1 activation had previously been shown to alter the cell cycle in hematopoietic progenitor cells and to delay their commitment to the myeloid lineage, a direct link between Notch1 and cell cycle control pathways had not been established in these cells.. Sarmento et al. now find the link and show that constitutive Notch1 activation drives cell cycling by increasing the activity of cyclin-dependent kinase-2 (CDK2), a protein that promotes progression into the S phase of the cell cycle. CDK2 activation resulted from the ...
Folia Histochemica et Cytobiologica (FHC) is an international,English-language journal devoted to the developing fields of histochemistry,cytochemistry,cell biology,cell and tissue biology.It is source of the recent research in fields of and cell biology
Human Crif1 is a protein with multiple functions, playing important roles in embryonic development, cellular stress, cell cycle regulation and mitochondrial membrane integrity. CRIF1 is coined to play a regulatory role in the Bone Marrow microenvironment-induced leukemia cell cycle arrest possibly through interacting with CDK2 and acting as a cyclin-dependent kinase inhibitor ...
Telomere attrition is usually a natural process that occurs due to inadequate telomere maintenance. expansion of DC cells can become partially overcome PD173074 by reducing O2 pressure from 21% to 4%. Further, repairing telomerase activity or inhibiting p53 or p21WAF/CIP significantly mitigated growth inhibition as well as caused a significant decrease in steady-state levels of superoxide. Our results support a model in which telomerase insufficiency in DC prospects to p21WAF/CIP signaling, p53, to cause improved steady-state levels of superoxide, metabolic oxidative stress, and senescence. 14, 985C997. Intro Cellular ageing entails the connection between biological ...
LONDON - During the recent past, Cyclin Dependent Kinase (CDK) Inhibitors have emerged as one of the most promising therapeutics for cancer and also a novel frontier for organiations engaged in the R&D, licensing and commercialisation of targeted cancer therapies.. Today, there are two CDK inhibitors commercially available in the cancer treatment market. Furthermore, there are over 45 CDK inhibitors in different phases of clinical development.. The recent remarkable advancements in the discovery of new cyclin pathways and their inhibitors have opened up novel prospects in the CDKs therapy ...
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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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Cardiac hypertrophy leading to heart failure remains a leading cause of morbidity and mortality in the 21st century despite major therapeutic advances. Improved understanding of novel molecular and cellular processes contributing to cardiac hypertrophy therefore continues to be important. Cyclin-dependent Kinase 9 (CDK9), part of a family of proteins controlling cell cycle and growth, has emerged as one such potential candidate over the last 5 years. CDK9 is the catalytic subunit of the CDK9/CyclinT complex and acts by phosphorylating the carboxy-terminal domain of RNA polymerase II. ...
Irreversible growth arrest is an early and integral part of squamous cell differentiation in normal human epidermal keratinocytes (NHEKs) and is assumed to be linked to the control of expression of differentiation-specific genes. In this study, we examine the link between the molecular events associated with growth arrest and the expression of differentiation genes. NHEKs that have been induced to undergo growth arrest and differentiation by suspension culture contain populations in both G1 and G2/M of the cell cycle. The irreversible growth arrest state in NHEKs is characterized by an accumulation of the hypophosphorylated forms of Rb and p130, with subsequent down-regulation of levels of Rb, up-regulation of p130 and associated ...
The p27Kip1 gene codes for a cyclin-dependent kinase inhibitor implicated in G1 arrest by transforming growth factor β, cell-cell contact, agents that elevate cyclic AMP, and the growth-inhibitory drug rapamycin. p27 binds to and inhibits complexes formed by cyclin E-cdk2, cyclin A-cdk2, and cyclin D-cdk4. The involvement of p27 in the negative regulation of cell proliferation suggests that it may also function as a tumor suppressor gene. Using a combination of somatic cell hybrid panels and fluorescence in situ hybridization ...
2VTH: Identification of N-(4-piperidinyl)-4-(2,6-dichlorobenzoylamino)-1H-pyrazole-3-carboxamide (AT7519), a Novel Cyclin Dependent Kinase Inhibitor Using Fragment-Based X-Ray Crystallography and Structure Based Drug Design
p35 is an activating co-factor of Cyclin-dependent kinase 5 (Cdk5), a protein whose dysfunction has been implicated in a wide-range of neurological disorders including cognitive impairment and disease. Inducible deletion of the p35 gene in adult mice results in profound deficits in hippocampal-dependent spatial learning and synaptic physiology, however the impact of the loss of p35 function on hippocampal in vivo physiology and spatial coding remains unknown. Here, we recorded CA1 pyramidal cell activity in freely behaving ...
Results: In vitro studies showed a pronounced growth inhibitory and pro-apoptotic effect of LBH589 on both HCC cell lines at low micromolar concentrations (IC50 approx. 0.1 µM). Interstingly, the pro-apoptotic effect of Panobinostat was not paralleled by a breakdown of ΔΨm. p53wt HepG2 cells were more sensitive than the p53-/- Hep3B cells. Quantitative PCR and western blotting showed an involvement of the cell cycle regulators p21cip1/waf1 and Chek1 but not the bax/bcl-2 system. Panobinostat regulated the expression of p21cip1/waf1 via a transcriptional upregulation as evidenced by ...
Cell proliferation is essential for many key processes that occur during development including organogenesis, tissue renewal and germline formation. (Bartkova et al., 1997; Clurman and Roberts, 1995; Pines, 1995; Sandhu and Slingerland, 2000). Therefore, the timing of cell division and differentiation must be precisely coordinated with signals that specify morphogenesis, patterning and growth in a temporal, positional and cell type-specific manner (reviewed by Vidwans and Su, 2001). This coordination is executed through regulating both positive and negative regulatory components of the basal cell cycle machinery.. The cell cycle machinery is well conserved among eukaryotes and complex mechanisms ensure that cell cycle ...
Due to its role in aging and antitumor defense, cellular senescence has recently attracted increasing interest. However, [the] detection of senescent cells remains difficult due to the lack of specific biomarkers. ndeed, most determinants of cellular senescence, such as the upregulation of p53, p16Ink4a, p21WAF/CIP1 or SASP-associated cytokines, are not exclusively observed in senescence, but can also occur in other types of stress responses. In addition, alterations like SAHF or DNA-SCARS formation are frequently observed, but not necessarily a mandatory feature or exclusive to senescent cells. The current gold standard for the detection of senescence is the so-called senescence-associated β-galactosidase (SA-β-Gal) activity. Although SA-β-Gal has been first suggested as a distinct enzyme, its activity is derived from lysosomal β-Gal encoded by the GLB1 ...
1OIT: Imidazo[1,2-A]Pyridines: A Potent and Selective Class of Cyclin-Dependent Kinase Inhibitors Identified Through Structure-Based Hybridisation
The goal of this study was to identify the structural elements within the cytoplasmic domains of human IL-31Rα that determines the four response categories of IL-6 cytokines in epithelial cells: (a) the ligand-dependent activation of signal transduction pathways, (b) altered expression of cytokine-responsive genes, (c) suppression of proliferation and (d) changes in cell morphology. In the first part of this study, using the human alveolar epithelial cell line A549 with an increased IL-31Rα expression, we were able to identify signaling specificity of the IL-31 cytokine defined by a prominent activation of STAT3, as well as the MAPK pathways: ERK1/2 and JNK, as well as Akt. ...
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Looking for exogenous p? Find out information about exogenous p. A group of substances thought to be polysaccharides of microbial origin that produce an increase in body temperature when injected into humans and some animals Explanation of exogenous p
K17002 MIR17; microRNA 17 K17003 MIR18A; microRNA 18a K17005 MIR19; microRNA 19 K17005 MIR19; microRNA 19 K17006 MIR20A; microRNA 20a K17008 MIR92A; microRNA 92a K01110 PTEN; phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN [EC:3.1.3.16 3.1.3.48 3.1.3.67] K17010 MIR221; microRNA 221 K17011 MIR222; microRNA 222 K06624 CDKN1B; cyclin-dependent kinase inhibitor 1B K16866 TIMP3; metalloproteinase inhibitor 3 K16980 MIRLET7; microRNA let-7 K16980 MIRLET7; microRNA let-7 K16980 MIRLET7; microRNA let-7 K16980 MIRLET7; microRNA let-7 K16980 MIRLET7; microRNA let-7 K17397 MIRLET7C; microRNA let-7c K07827 KRAS; ...
Cellular senescence is a fundamental cell fate playing significant and complex roles during tumorigenesis and natural aging process. However, the molecular determinants distinguishing senescence from other temporary and permanent cell-cycle arrest states such as quiescence and post-mitotic state and the specified mechanisms underlying cell-fate decisions towards senescence versus cell death in response to cellular stress stimuli remain less understood. In our studies, we aimed to employ multi-omics approaches to deepen our understanding of cellular senescence, in particular, regarding the specific molecular determinants distinguishing cellular senescence from other non-dividing cell fates. Notably, one of the most prominent features of ...
2VTN: Identification of N-(4-Piperidinyl)-4-(2,6-Dichlorobenzoylamino)-1H-Pyrazole-3-Carboxamide (at7519), a Novel Cyclin Dependent Kinase Inhibitor Using Fragment-Based X-Ray Crystallography and Structure Based Drug Design.
p27/Kip1 antibody to detect human cyclin-dependent kinase inhibitor 1. Validated on up to 12 cell lysates for western blotting. Try a trial size today.
If you have a question about this talk, please contact Caroline Newnham.. Host: Viji Draviam. Tissue homeostasis in metazoans is regulated by transitions of cells between quiescence and proliferation. The hallmark of proliferating populations is progression through the cell cycle, which is driven by Cyclin-dependent kinase (CDK) activity. I will discuss our recent development of a live-cell sensor for CDK2 activity and the finding that proliferating cells bifurcate into two populations as they exit mitosis. Some cells immediately commit to the next cell cycle by building up CDK2 activity from an intermediate level, while other cells lack CDK2 activity and enter a transient state of ...
Cyclin-dependent Kinase Inhibitor (CKI); Inhibitor Of Cdc28-Clb Kinase Complexes That Controls G1/S Phase Transition, Preventing Premature S Phase And Ensuring Genomic Integrity; Phosphorylated By Clb5/6-Cdk1 And Cln1/2-Cdk1 Kinase Which Regulate Timing Of Sic1p Degradation; Phosphorylation Targets Sic1p For SCF(CDC4)-dependent Turnover; Functional Homolog Of Mammalian Kip1
Cyclin-dependent kinase 4 (CDK4) is a member of cyclin-dependent kinase family which regulates G1 to S cell cycle transition. CDK4 activity is increased in many tumor types. Here, we report a...
Cancer develops due to an imbalance between cell proliferation and cell death. Various mechanisms of carcinogenesis as well as of novel anticancer agents that could be targeted for the treatment of cancer have been proposed by different studies. Among these, p21 is recognized as a potent cyclin-dependent kinase inhibitor that facilitates cell-cycle arrest by interacting with different stimuli such as p53, DNA repair process, CDK, E2F1, MYC, PCNA, STAT3 AP4, proteasomes, K1F, CDX2, and ER-α. p21 acts both as a tumor-suppressor gene and an inhibitor of apoptosis by interacting ...
Chronic lymphocytic leukemia (CLL) cells multiply and become more resistant to immunochemotherapy in "proliferation centers" within tissues, whereas apoptosis occurs in the periphery. Various models recapitulate these microenvironments in vitro, such as stimulation with CD154 and IL4. Using this system, we observed a 30- to 40-fold induction of wild-type p53 protein in 50 distinct human CLL specimens tested, without the induction of either cell-cycle arrest or apoptosis. In contrast, the mRNA levels for p53 did not increase, indicating that its elevation occurred posttranscriptionally. Mechanistic investigations revealed that under the conditions studied, p53 was ...
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)
Dinaciclib, also known as SCH727965, is a potent CDK inhibitor with potential antineoplastic activity. Dinaciclib selectively inhibits cyclin dependent kinases CDK1, CDK2, CDK5, and CDK9 activity in vitro with IC(50) values of 1, 1, 3, and 4 nmol/L, respectively. Compared with flavopiridol, Dinaciclib exhibits superior activity with an improved therapeutic index. Dinaciclib induced regression of established solid tumors in a range of mouse models following intermittent scheduling of doses below the maximally tolerated level..
Schematic of the cell cycle. outer ring: I=Interphase, M=Mitosis; inner ring: M=Mitosis; G1=Gap phase 1; S=Synthesis; G2=Gap phase 2. The duration of mitosis in relation to the other phases has been exaggerated in this diagram Cyclin dependent
The cell cycle is under strict regulation. Cyclin-dependent kinases (CDKs) at the G1-S and G2-M checkpoints are positively regulated by cyclins and negatively regulated b..
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 ...
Cyclin-dependent kinases (CDKs) are core components of the cell cycle machinery that govern the transition between phases during cell cycle progression. Genes involved in cell cycle are frequently mutated in human cancer and deregulated CDK activity repr
MONARCH 1: Final overall survival analysis of a phase 2 study of abemaciclib, a CDK4 and CDK6 inhibitor, as monotherapy, in patients with HR+/HER2- breast cancer, after chemotherapy for advanced ...
1KE9: Oxindole-based inhibitors of cyclin-dependent kinase 2 (CDK2): design, synthesis, enzymatic activities, and X-ray crystallographic analysis.
p15 INK4b antibody, Internal (cyclin-dependent kinase inhibitor 2B) for WB. Anti-p15 INK4b pAb (GTX77673) is tested in Human samples. 100% Ab-Assurance.
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 ...
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 ...
Throughout the one-hour discussion, Kip kept talking about the vital importance of treating employees well. Kip believes companies have a "moral authority" to make the work environment such that employees go to work because they want to, not have to.. [SIDEBAR: Kip said Fortune Magazine had a difficult time believing such a small, regional company could rank so high on their "annual best companies to work for" list. The magazine ended up sending a reporter to work in a store for a few weeks to learn what was going.]. Today, The Container Store truly does treat its employees well. The average store-level employee at The Container Store makes $48,000 a year. Thats twice as much as someone could expect to get paid for a similar job ...
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 ...
Effects of exogenous p62-overexpression. (a) H23 cells were transfected with indicated siRNAs for 3 days. After transfection, cell viability was measured, and
Cdk5r1 - Cdk5r1 (Myc-DDK-tagged ORF) - Rat cyclin-dependent kinase 5, regulatory subunit 1 (p35) (Cdk5r1), (10 ug) available for purchase from OriGene - Your Gene Company.
Cdk14 - Cdk14 (Myc-DDK-tagged) - Mouse cyclin-dependent kinase 14 (Cdk14) available for purchase from OriGene - Your Gene Company.
HMN-214 inhibits polo-like and cyclin-dependent kinase activity, has potent antimicrotubular effects and results in profound apoptosis and antitumor activity in a broad spectrum of human xenografts.
Gold CIP Processing,Gold CIP Plant,Gold CIP Production Line.MES CIP Production Line has helped hundreds of mines to recover gold.Gold Carbon in pulp (CIP) production is the sequent
(KudoZ) English to Bosnian translation of EURO parity CIP : (cijene...) u EUR na paritetu CIP... [Finance (general) (Bus/Financial)].
SDI2 allows scientists to see precisely whats happening at the solid-liquid interface during the dissolution process. Learn more about this unique tool.
高い抗原親和性、特異性と安定した品質を兼ね備えたアブカムのウサギ・モノクローナル抗体 RabMAb® ab92741 交差種: Ms,Rat 適用: WB,IHC-P

CDKN2A - Humpath.com - Human pathologyCDKN2A - Humpath.com - Human pathology

P16, INK4, INK4A, CYCLIN-DEPENDENT KINASE INHIBITOR 2A, CDKN2A Definition: p16 is an inhibitor of cyclin-dependent kinases. ... p16INK4 gene encodes a specific inhibitor of cyclin-dependent kinase 4 (CDK4). p16INK4a binds to cyclin D-CDK4 and promotes the ... Definition: p16 is an inhibitor of cyclin-dependent kinases. ... p16 protein, P16, INK4, INK4A, CYCLIN-DEPENDENT KINASE ... Since the CDK4/cyclin D complex propels a cell to go through the G1 check point of the cell cycle, a critical phase of cell ...
more infohttp://www.humpath.com/spip.php?article2209

In vitro drug resistance and prognostic impact of p16INK4A/P15INK4B deletions in childhood T-cell acute lymphoblastic leukaemia...In vitro drug resistance and prognostic impact of p16INK4A/P15INK4B deletions in childhood T-cell acute lymphoblastic leukaemia...

... p16INK4a protein is an inhibitor of cyclin-dependent-kinase 4 (CDK4), thus blocking the cell cycle at the G1 phase through the ... Detection of homozygous deletions of the cyclin-dependent kinase 4 inhibitor (p16) gene in acute lymphoblastic leukemia and ... p19 ARF interacts with Mdm-2 resulting in a reversal of the inhibitory binding of Mdm-2 to the p53 protein (Kamijo et al, 1998 ... Analysis of a family of cyclin-dependent kinase inhibitors: p15/MTS2/INK4B, p16/MTS1/INK4A, and p18 genes in acute ...
more infohttp://onlinelibrary.wiley.com/doi/10.1046/j.1365-2141.2001.02586.x/full

New Page 2New Page 2

cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4). * CMM2. * CDKN2. * CDK4I ... p16(INK4a) (p16) is tight-binding and inhibitory protein for cyclin-dependent kinase 4. Kobayashi S, Shirasawa H, Sashiyama H, ... Mutation of cell cycle regulators, such as inhibitor of CDK4 or p16 tumor suppressor gene, is a new molecular event in pancreas ... Regulators of the G1 checkpoint include an inhibitor of cyclin-dependent kinase, p16INK4. Okamoto A, Demetrick DJ, Spillare EA ...
more infohttp://bioinformatics.org/pcgdb/Genes/cdkn2a/cdkn2a.htm

P16 - WikipediaP16 - Wikipedia

"Entrez Gene: CDKN2A cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4)". Nobori T, Miura K, Wu DJ, Lois A, ... p16 acts as a tumor suppressor by binding to CDK4/6 and preventing its interaction with cyclin D. This interaction ultimately ... p16 is also known as: p16Ink4A p16Ink4 Cyclin-dependent kinase inhibitor 2A (CDKN2A) CDKN2 CDK 4 Inhibitor Multiple Tumor ... p16 is a cyclin-dependent kinase (CDK) inhibitor that slows down the cell cycle by prohibiting progression from G1 phase to S ...
more infohttps://en.wikipedia.org/wiki/P16

Characterization and Prospective of Human Corneal Endothelial ProgenitorsCharacterization and Prospective of Human Corneal Endothelial Progenitors

CDK4) and cyclin E/CDK2 complex, but negatively by cyclin-dependent kinase inhibitors (CKIs) such as p16INK4a, p15INK4b, p18 ... Nuclear p16INK4a is a hallmark of contact inhibition because p16INK4a binds to CDK4/6 inhibiting its kinase activity thereby ... Cellular senescence and tumor suppressor gene p16. Int J Cancer. 2012;130:1715-25 ... p16INK4a: a tumor suppressor protein functions as an inhibitor of CDK4 and CDK6, the D-type cyclin-dependent kinases that ...
more infohttp://www.medsci.org/v14p0705.htm

The anti-tumor efficacy of CDK4/6 inhibition is enhanced by the combination with PI3K/AKT/mTOR inhibitors through impairment of...The anti-tumor efficacy of CDK4/6 inhibition is enhanced by the combination with PI3K/AKT/mTOR inhibitors through impairment of...

Palbociclib is a selective inhibitor of the cyclin-dependent kinases 4 and 6 (CDK4/6), which... ... p16INK4 is a cyclin-dependent kinase inhibitor (CDKI), that blocks the binding site of cyclin D1 on CDK4/6. Loss of functional ... due to both mutation or homozygous loss of the gene, may be observed in all BC subtypes, with a higher frequency in TNBC (7-20 ... Palbociclib is a selective inhibitor of the cyclin-dependent kinases 4 and 6 (CDK4/6), which coordinate the G1-S transition. ...
more infohttps://link.springer.com/article/10.1186/s13046-018-0741-3

Molecular background of skin melanoma development and progression: therapeutic implications
	Molecular background of skin melanoma development and progression: therapeutic implications

p16 is coded by CDKN2A (cyclin dependent kinase inhibitor 2A) gene mutated in 40-50% of melanoma cases [40, 41]. Inactivation ... It activates RB protein by binding and inhibiting cyclin dependent kinase 4 (CDK4) [44] thus inhibition of CDK4 is being tested ... PD-1 is a T-cell co-inhibitor receptor activated through the binding with two ligands, PD-L1 (B7-H1, CD274) and PD-L2 (CD273). ... expression of its inhibitor, ID1, and activation of WNT/-catenin pathway [43]. p16 protein is an RB activator and protects the ...
more infohttps://www.termedia.pl/Molecular-background-of-skin-melanoma-development-and-progression-therapeutic-implications,7,36440,1,1.html

Index: pIndex: p

p16INK4a. p16INK4a is a tumor-suppressor which inhibits the cyclin-dependent kinases 4 and 6. Its inhibitory effect results ... from its binding to CDk4/6 and by this preventing the formation of the Cdk4/6-cyclin D complex. INK4 inhibitors (p16INK4a and ... p14ARF (or just ARF) is a human tumor-suppressor gene (the mouse homolog is p19ARF); it is activated by E2F-1 and stabilizes ... Cyclin-dependent kinase Inhibitor Protein), suggesting a direct link between p53, negative regulation of the kinases required ...
more infohttp://celldeath.de/encyclo/index/p.htm

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 ... Cyclin-dependent kinase 4 also known as cell division protein kinase 4 is an enzyme that in humans is encoded by the CDK4 gene ... cyclin-dependent protein serine/threonine kinase regulator activity. • protein binding. • ATP binding. • cyclin binding. • ... CDK4, CMM3, PSK-J3, cyclin-dependent kinase 4, cyclin dependent kinase 4. ...
more infohttps://en.wikipedia.org/wiki/CDK4

Phenotypic and Molecular Characterization of MCF10DCIS and SUM Breast Cancer Cell LinesPhenotypic and Molecular Characterization of MCF10DCIS and SUM Breast Cancer Cell Lines

... and the kinase activity of CDK4 is suppressed by p16INK4a (p16). Cyclin-dependent kinase inhibitor 2A, (CDKN2A, ) also known as ... which bind to and activate cyclin-dependent kinases (CDK4 and CDK6) as shown in Figure 5. These complexes lead to the ... "Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers," Nature, vol. 368, no. 6473, pp. 753-756, ... p21 is a potent cyclin-dependent kinase inhibitor and inhibits the activity of cyclin-CDK2 or -CDK1 complexes, and thus ...
more infohttps://www.hindawi.com/journals/ijbc/2013/872743/

Molecular pathogenesis of oral squamous carcinoma | Molecular PathologyMolecular pathogenesis of oral squamous carcinoma | Molecular Pathology

p16INK4 binds to and inhibits phosphorylation of pRb by the cyclin dependent kinases CDK4 and CDK6.22,23 ... The cyclin dependent kinase inhibitor 2/multiple tumour suppressor gene 1 (CDKN2/MTSI) has been mapped to this chromosome ... 21 Cyclins, cyclin dependant kinases (CDKs), and cyclin dependent kinase inhibitors regulate progress through key transitions ... encoded by the WAF1/CIP gene, p21 being an inhibitor of cyclin and cyclin dependant kinase complexes.60 p21 transcription is ...
more infohttp://mp.bmj.com/content/53/4/165

Cyclin D - WikipediaCyclin D - Wikipedia

... activate cyclin D gene in response to integrin. p27kip1 and p21cip1 are cyclin-dependent kinase inhibitors (CKIs) which ... P16 functions in inactivating cyclin D/Cdk 4 complex. Thus, blocking transcription of INK4 gene would increase cyclin D/Cdk4 ... Hence, INK4 binds to cyclin D- dependent CDKs and inactivates the whole complex. Glycogen synthase kinase three beta, GSK3β, ... Inactivation of cyclin D is triggered by several cyclin-dependent kinase inhibitor protein (CKIs) like the INK4 family (e.g. ...
more infohttps://en.wikipedia.org/wiki/Cyclin_D

p16INK4a detectionp16INK4a detection

p16INK4a is a cyclin-dependent kinase (CDK) inhibitor, and binds CDK4 and CDK6 and inhibits their kinase activity. It is also ... The human cyclin-dependent kinase inhibitor 2A (CDKN2A) gene generates several transcript variants that differ in their first ... p16, inhibits CDK4); cyclin-dependent kinase inhibitor 2A, CDKN2A, cyclin-dependent kinase 4 inhibitor A, CDK4 inhibitor p16- ... p16INK4a is a cyclin-dependent kinase (CDK) inhibitor, and binds CDK4 and CDK6 and inhibits their kinase activity. It is also ...
more infohttps://www.takarabio.com/products/antibodies-and-elisa/primary-antibodies-and-elisas-by-research-area/cancer-and-inflammation/p16ink4a

Expression of P16 in high-risk human papillomavirus related lesions of the uterine cervix in a government hospital, Malaysia |...Expression of P16 in high-risk human papillomavirus related lesions of the uterine cervix in a government hospital, Malaysia |...

p16 expression was strongly observed in cervical cancer and minimally observed in cervicitis. Thus indicating p16 ... The immunohistochemical staining with p16 and HPV 16 L1 were done on all cases. The staining intensity and density were ... The current study aims to evaluate the diagnostic value of p16 immunohistochemical (IHC) investigation in high-risk human ... The p16 gene is on chromosome 9p21-22, and maps for a cyclin dependent kinase (cdk)-4 inhibitor. It normally decelerates the ...
more infohttps://diagnosticpathology.biomedcentral.com/articles/10.1186/s13000-014-0202-z

anti-p21 Cip1 antibody  | GeneTexanti-p21 Cip1 antibody | GeneTex

... cyclin-dependent kinase inhibitor 1A (p21, Cip1)) for IHC-Fr, IP, WB. Anti-p21 Cip1 pAb (GTX27960) is tested in Human, Mouse, ... cyclin-dependent kinase inhibitor 1A (p21, Cip1). Background. Cell cycle progression is regulated by cyclins and their cognate ... like cyclin D1/Cdk4 (4,8). An additional CDI has been found to bind Cdk4 and Cdk6, p16 (INK4A), and when such complexes are ... It has become increasingly clear that p16 is a very important tumor suppressor gene whose frequent loss occurs early in many ...
more infohttp://www.genetex.com/p21-Cip1-antibody-GTX27960.html

Hepatoepigenetic Alterations in Viral and Nonviral-Induced Hepatocellular CarcinomaHepatoepigenetic Alterations in Viral and Nonviral-Induced Hepatocellular Carcinoma

... p16ink4α/cyclin dependent kinase inhibitor 2A (CDKN2A), p15, suppressor of the cytokine signalling 1 (SOCS1), E-cadherin (CHD1 ... and zinc finger E-box binding homeobox 1 [79-84]. In particular, miR-145 was found to function as a tumour suppressor gene and ... protein attaches to cyclin dependent kinase- (CDK-) 4 or CDK-6 to inhibit cell cycle progression. The p1. protein protects p53 ... Cyclin dependent kinase inhibitor 2A (CDKN2A) was identified as a target of repression by H3K27me3 mediated by upregulation in ...
more infohttps://www.hindawi.com/journals/bmri/2016/3956485/

CDKN2A (p16) - Chordoma FoundationCDKN2A (p16) - Chordoma Foundation

Substrates: CDK4/6. p16 is a tumor suppressor that functions by binding to cyclin-dependent kinases (CDK4/6) and preventing ... CDKN2A (p16) The CDKN2A gene produces the p16 protein. The protein is a critical player in the cell cycle, blocking a cells ... Abemaciclib: Treatment of U-CH1 and U-CH2 with CDK4/6 inhibitor Abemaciclib (LY2835219) reduced cell viability.4 ... for inhibition of the CDK4/6 cyclin dependent kinase pathways by pharmacological agents.16 ...
more infohttps://www.chordomafoundation.org/targets/p16/

Long noncoding RNA PVT1 indicates a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically...Long noncoding RNA PVT1 indicates a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically...

... and that this association was required for the repression of p15 and p16. To our knowledge, this is the first report showed ... p15 and p16 belong to INKs family of cyclin-dependent kinase (cdk) inhibitor proteins; they bind to cycilnD either alone or ... And p15 and p16 act as tumor suppressors in various cancers, and aberrant methylation in p15 and p16 gene promoter region has ... when complexed to their caralytic subunit CDK4 and prevent the activation of cyclinD-CDK4 complexes, and thus control the cell ...
more infohttps://molecular-cancer.biomedcentral.com/articles/10.1186/s12943-015-0355-8

The Xenopus cyclin-dependent kinase inhibitor Ink4d is functionally conserved with murine p19Ink4d and is required for neural...The Xenopus cyclin-dependent kinase inhibitor Ink4d is functionally conserved with murine p19Ink4d and is required for neural...

Inhibitors of Cdk4). The Ink4 family of CKIs consists of four members; p16Ink4a, p15Ink4b, p18Ink4c and p19Ink4d, and they bind ... Paper III describes the cloning and characterization of a gene homologous to Ink4d, Xl-Ink4d. This CKI is expressed throughout ... The Xenopus cyclin-dependent kinase inhibitor Ink4d is functionally conserved with murine p19Ink4d and is required for neural ... Progression through the G1, S, G2 and M phases of the cell cycle is controlled by cyclin-dependent kinases (Cdks) and cyclins. ...
more infohttp://umu.diva-portal.org/smash/record.jsf?pid=diva2:140747

CDK4/6 - Chordoma FoundationCDK4/6 - Chordoma Foundation

CDK4/6 Cyclin-dependent kinase 4 (CDK4) and Cyclin-dependent kinase 6 (CDK6) are serine-threonine kinases that regulate cell ... CDK4 and CDK6 (CDK4/6) are frequently overactivated in chordoma due to loss of the CDK4/6 inhibitor CDKN2A (p16). CDKN2A and ... CDK4/6 bind to D-type cyclins to accelerate cells toward S phase in the cell cycle. The primary role of CDK4/6 is to ... CDK4 and CDK6 are oncoproteins that are normally controlled by the CDKN2A gene (p16 protein). Upregulation of CDK4/6 or ...
more infohttps://www.chordomafoundation.org/targets/cdk46/

Inhibition of Breast Tumor Cell Growth by Ectopic Expression of p16/INK4A Via Combined Effects of Cell Cycle Arrest, Senescence...Inhibition of Breast Tumor Cell Growth by Ectopic Expression of p16/INK4A Via Combined Effects of Cell Cycle Arrest, Senescence...

p16 downregulates CDK4 expression. p16 is a cyclin-dependent kinase (CDK4/6) inhibitor and a negative cell cycle regulator: by ... and our ongoing studies revealed that p16 directly binds to HIF-1α, the transcriptional regulator of the VEGF gene, and alters ... Concomitant presence of p16/cyclin-dependent kinase 4 and cyclin D/cyclin-dependent kinase 4 complexes in LNCaP prostatic ... The tumor suppressor gene p16 (also called MTS1, CDKN2 and INK4A) is a cyclin-dependent kinase (CDK) inhibitor and a negative ...
more infohttp://jcancer.org/v03p0333.htm

Specific inhibition of cyclin-dependent kinase 4/6 by PD 0332991 and associated antitumor activity in human tumor xenografts |...Specific inhibition of cyclin-dependent kinase 4/6 by PD 0332991 and associated antitumor activity in human tumor xenografts |...

... down-regulation of a naturally occurring inhibitor of Cdk4, called p16INK4A; mutations in Cdk4 that prevent p16INK4A binding to ... The only known natural substrates for Cdk4/6 are the Rb family of gene products, p110(Rb), p107, and p130 (76). Of the 16 known ... A potent inhibitor of the cyclin D-dependent kinases CDK4 and CDK6. J Biol Chem 2001;276:16617-23. ... PD 0332991 is a highly specific inhibitor of cyclin-dependent kinase 4 (Cdk4) (IC50, 0.011 μmol/L) and Cdk6 (IC50, 0.016 μmol/L ...
more infohttp://mct.aacrjournals.org/content/3/11/1427.long

Familiäres Melanom | Springer for Research & DevelopmentFamiliäres Melanom | Springer for Research & Development

Novel mutations in the p16/CDKN2A binding region of the cyclin-dependent kinase-4 gene. Cancer Res 58:109-113PubMedGoogle ... Nobori T, Miura K, Wu DJ, Lois A, Takabayashi K, Carson DA (1994) Deletions of the cyclin-dependent kinase-4 inhibitor gene in ... 1997) p16/CDKN2 and CDK4 gene mutations in sporadic melanoma development and progression. Int J Cancer 74:26-30PubMedGoogle ... Wang Y, Becker D (1996) Differential expression of the cyclin-dependent kinase inhibitors p16 and p21 in the human melanocytic ...
more infohttps://rd.springer.com/chapter/10.1007/978-3-642-56889-3_4

CDK4 elisa kit | Rat Cyclin Dependent Kinase 4 ELISA Kit-NP 000066.1CDK4 elisa kit | Rat Cyclin Dependent Kinase 4 ELISA Kit-NP 000066.1

Rat Cyclin Dependent Kinase 4 ELISA Kit-NP_000066.1 (MBS2533543) product datasheet at MyBioSource, ELISA Kits ... Controlled by the regulatory subunits D-type cyclins and CDK inhibitor p16(INK4a). Phosphorylates the retinoblastoma gene ... Molecular Function: ATP binding; cyclin binding; cyclin-dependent protein kinase activity; cyclin-dependent protein kinase ... CDK4 elisa kit :: Rat Cyclin Dependent Kinase 4 ELISA Kit. Catalog #. MBS2533543 .mycenter { display: block; margin-left: auto ...
more infohttps://www.mybiosource.com/prods/ELISA-Kit/Rat/Cyclin-Dependent-Kinase-4/CDK4/datasheet.php?products_id=2533543&utm_source=TDSQR

The Drosophila Cyclin D-Cdk4 complex promotes cellular growth | The EMBO JournalThe Drosophila Cyclin D-Cdk4 complex promotes cellular growth | The EMBO Journal

MEFs from mice lacking p16INK4A, a specific inhibitor of CycD‐dependent kinases, also exhibit accelerated growth (Serrano et al ... Du W, Vidal M, Xie J‐E and Dyson N (1996a) RBF, a novel RB‐related gene that regulates E2F activity and interacts with cyclin E ... binding motif, LXCXE (underlined) and is 39% identical to human cyclins D1 and D2 at the amino acid level. A 2.1 kb NotI-KpnI ... Kato JY, Matsuoka M, Strom DK and Sherr CJ (1994) Regulation of cyclin D‐dependent kinase 4 (cdk4) by cdk4‐activating kinase. ...
more infohttp://emboj.embopress.org/content/19/17/4543
  • Inactivation of PARP during the execution phase of apoptosis by caspase cleavage might be necessary to prevent NAD+ and ATP depletion and thus to prevent a switch from an ATP-dependent apoptotic mode of cell death to an energy depletion-induced necrotic mode (Amours et al, 2001, J. Cell Science, 114(20) 3771-77). (celldeath.de)
  • Subsequently, cyclin E/Cdk2 fully phosphorylates Rb and completes its inactivation. (wikipedia.org)
  • The inactivation of p16 appears to be a common event in many cancers ( 2 - 9 ). (jcancer.org)
  • Risk of developing pancreatic cancer in families with familial atypical multiple mole melanoma associated with a specific 19 deletion of p16 (p16-Leiden). (bioinformatics.org)
  • 1989) Mapping the gene for hereditary cutaneous malignant melanoma-dysplastic nevus to chromosome 1p. (springer.com)
  • Interaction of viral products with the host cell machinery may lead to increased frequency of genetic and epigenetic aberrations that cause harmful alterations in gene transcription. (hindawi.com)
  • DNA methylation, histone modification, and noncoding miRNA are important epigenetic phenomena that collaboratively regulate gene expression and alter the normal function especially during pathological processes [ 7 - 10 ]. (hindawi.com)
  • They have been shown to regulate gene expression at multiple levels, including chromatin modification, transcription and post-transcriptional processing. (biomedcentral.com)
  • MicroRNAs (miRNA) regulate complex patterns of gene expression, and the relevance of altered miRNA expression to ovarian cancer remains to be elucidated. (aacrjournals.org)
  • Once phosphorylated, pRB disassociates from the transcription factor E2F1, liberating E2F1 from its cytoplasm bound state allowing it to enter the nucleus. (wikipedia.org)
  • PRC1 and PRC2 are two protein complexes that modify the expression of p16 through the interaction of various transcription factors that execute methylation patterns that can repress transcription of p16. (wikipedia.org)
  • Active cyclin D/Cdk4 and -6 inhibit Rb by partial phosphorylation, reducing its binding to E2F and thereby allowing E2F-mediated activation of the transcription of the cyclin E gene and the cell progresses towards S-phase. (wikipedia.org)
  • Presented are steps of the gene expression cycle of Lamin A / C that can be targeted for additional regulation: transcription, splicing, translation, posttranslational modification, and degradation via autophagy. (nih.gov)
  • This complex binds to rRNA gene promoters and may play a role in rRNA transcription and/or maturation. (thefreedictionary.com)
  • The synthesis of cyclin D is initiated during G1 and drives the G1/S phase transition. (wikipedia.org)
  • The current study aims to evaluate the diagnostic value of p16 immunohistochemical (IHC) investigation in high-risk human papillomavirus (HR-HPV) related lesions of the uterine cervix in Hospital Tuanku Jaafar, Seremban, Malaysia. (biomedcentral.com)
  • Functionally, miRNAs bind to complementary sequences in the 3′ untranslated region of target gene transcripts, leading to mRNA degradation and/or translational repression ( 6 ). (aacrjournals.org)
  • Our previous study demonstrated that introduction of exogenous p16 via adenoviral gene transfer downregulated VEGF expression and inhibited angiogenesis in human BCa cells ( 17 ). (jcancer.org)
  • p16 FISH deletion in surface epithelial mesothelial proliferations is predictive of underlying invasive mesothelioma . (humpath.com)
  • Homozygous deletion of p16 are frequently found in esophageal cancer and gastric cancer cell lines. (wikipedia.org)
  • The ELISA analytical biochemical technique of the MBS2533543 kit is based on CDK4 antibody-CDK4 antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect CDK4 antigen targets in samples. (mybiosource.com)
  • The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to CDK4. (mybiosource.com)
  • Only those wells that contain CDK4, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. (mybiosource.com)
  • p16 expression was strongly observed in cervical cancer and minimally observed in cervicitis. (biomedcentral.com)
  • Here, we generated comprehensive miRNA and gene expression profiles for ovarian cancer by comparing papillary serous ovarian cancers, the most common cause of ovarian cancer deaths in women, with established ovarian cancer cell lines and short-term primary cultures of normal ovarian surface epithelium (NOSE). (aacrjournals.org)
  • Gene therapy to improve the surgical therapeutic results for pancreas cancer. (bioinformatics.org)
  • As a first step toward identification of novel targets for therapeutic development, we used an integrative functional genomics approach that leverages the power of RNAi screens and multidimensional cancer genomics by The Cancer Genome Atlas (TCGA) to identify "druggable" kinases that are essential and transforming in GBM. (pnas.org)
  • Two mutant CDK4 isoforms (R24C, R24L) similarly stimulated T cell responses in vitro and were analyzed as therapeutic targets for TCR gene therapy. (jci.org)
  • The emerging data including ours indicated that p16 contributes its anti-cancer ability by inducing tumor cells to senescence. (jcancer.org)
  • p16 gene deletions are present in about 70% of primary paediatric T-cell acute lymphoblastic leukaemia (T-ALL) and 20% of common/precursor B-cell ALL cases. (wiley.com)
  • It is not clear what the impact of the frequent p16 deletions is within the subgroup of T-lineage ALL. (wiley.com)
  • We studied the relationship between p16/p19 ARF deletions, using fluorescence in situ hybridization, and in vitro drug resistance and prognosis in childhood T-ALL at diagnosis. (wiley.com)
  • All of these aberrations can lead to loss of proliferative controls either through elimination of the checkpoint altogether or through inappropriate or enhanced Cdk4 activity resulting in hyperphosphorylation of Rb. (aacrjournals.org)
  • therefore, this study justifies and promotes the viral-mediated p16 gene therapy as a promising and powerful treatment approach for cancer patients due to p16's multiple anti-tumor functions. (jcancer.org)
  • We find that Drosophila CycD-Cdk4 does not act as a direct G 1 /S‐phase regulator, but instead promotes cellular growth (accumulation of mass). (embopress.org)