A cyclin-dependent kinase inhibitor that coordinates the activation of CYCLIN and CYCLIN-DEPENDENT KINASES during the CELL CYCLE. It interacts with active CYCLIN D complexed to CYCLIN-DEPENDENT KINASE 4 in proliferating cells, while in arrested cells it binds and inhibits CYCLIN E complexed to CYCLIN-DEPENDENT KINASE 2.
A cyclin-dependent kinase inhibitor that mediates TUMOR SUPPRESSOR PROTEIN P53-dependent CELL CYCLE arrest. p21 interacts with a range of CYCLIN-DEPENDENT KINASES and associates with PROLIFERATING CELL NUCLEAR ANTIGEN and CASPASE 3.
Protein kinases that control cell cycle progression in all eukaryotes and require physical association with CYCLINS to achieve full enzymatic activity. Cyclin-dependent kinases are regulated by phosphorylation and dephosphorylation events.
A large family of regulatory proteins that function as accessory subunits to a variety of CYCLIN-DEPENDENT KINASES. They generally function as ENZYME ACTIVATORS that drive the CELL CYCLE through transitions between phases. A subset of cyclins may also function as transcriptional regulators.
Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.
A product of the p16 tumor suppressor gene (GENES, P16). It is also called INK4 or INK4A because it is the prototype member of the INK4 CYCLIN-DEPENDENT KINASE INHIBITORS. This protein is produced from the alpha mRNA transcript of the p16 gene. The other gene product, produced from the alternatively spliced beta transcript, is TUMOR SUPPRESSOR PROTEIN P14ARF. Both p16 gene products have tumor suppressor functions.
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
Proteins that are normally involved in holding cellular growth in check. Deficiencies or abnormalities in these proteins may lead to unregulated cell growth and tumor development.
High molecular weight proteins found in the MICROTUBULES of the cytoskeletal system. Under certain conditions they are required for TUBULIN assembly into the microtubules and stabilize the assembled microtubules.
A key regulator of CELL CYCLE progression. It partners with CYCLIN E to regulate entry into S PHASE and also interacts with CYCLIN A to phosphorylate RETINOBLASTOMA PROTEIN. Its activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P27 and CYCLIN-DEPENDENT KINASE INHIBITOR P21.
Protein encoded by the bcl-1 gene which plays a critical role in regulating the cell cycle. Overexpression of cyclin D1 is the result of bcl-1 rearrangement, a t(11;14) translocation, and is implicated in various neoplasms.
A cyclin subtype that has specificity for CDC2 PROTEIN KINASE and CYCLIN-DEPENDENT KINASE 2. It plays a role in progression of the CELL CYCLE through G1/S and G2/M phase transitions.
A 50-kDa protein that complexes with CYCLIN-DEPENDENT KINASE 2 in the late G1 phase of the cell cycle.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Cyclin-dependent kinase 4 is a key regulator of G1 PHASE of the CELL CYCLE. It partners with CYCLIN D to phosphorylate RETINOBLASTOMA PROTEIN. CDK4 activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P16.
A family of cell cycle-dependent kinases that are related in structure to CDC28 PROTEIN KINASE; S CEREVISIAE; and the CDC2 PROTEIN KINASE found in mammalian species.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A potent inhibitor of CYCLIN-DEPENDENT KINASES in G1 PHASE and S PHASE. In humans, aberrant expression of p57 is associated with various NEOPLASMS as well as with BECKWITH-WIEDEMANN SYNDROME.
A cell line derived from cultured tumor cells.
Agents that inhibit PROTEIN KINASES.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
The period of the CELL CYCLE preceding DNA REPLICATION in S PHASE. Subphases of G1 include "competence" (to respond to growth factors), G1a (entry into G1), G1b (progression), and G1c (assembly). Progression through the G1 subphases is effected by limiting growth factors, nutrients, or inhibitors.
A serine-threonine kinase that plays important roles in CELL DIFFERENTIATION; CELL MIGRATION; and CELL DEATH of NERVE CELLS. It is closely related to other CYCLIN-DEPENDENT KINASES but does not seem to participate in CELL CYCLE regulation.
A cyclin subtype that is transported into the CELL NUCLEUS at the end of the G2 PHASE. It stimulates the G2/M phase transition by activating CDC2 PROTEIN KINASE.
A cyclin subtype that is specific for CYCLIN-DEPENDENT KINASE 4 and CYCLIN-DEPENDENT KINASE 6. Unlike most cyclins, cyclin D expression is not cyclical, but rather it is expressed in response to proliferative signals. Cyclin D may therefore play a role in cellular responses to mitogenic signals.
Phosphoprotein with protein kinase activity that functions in the G2/M phase transition of the CELL CYCLE. It is the catalytic subunit of the MATURATION-PROMOTING FACTOR and complexes with both CYCLIN A and CYCLIN B in mammalian cells. The maximal activity of cyclin-dependent kinase 1 is achieved when it is fully dephosphorylated.
A group of cell cycle proteins that negatively regulate the activity of CYCLIN/CYCLIN-DEPENDENT KINASE complexes. They inhibit CELL CYCLE progression and help control CELL PROLIFERATION following GENOTOXIC STRESS as well as during CELL DIFFERENTIATION.
A cyclin subtype that binds to the CYCLIN-DEPENDENT KINASE 3 and CYCLIN-DEPENDENT KINASE 8. Cyclin C plays a dual role as a transcriptional regulator and a G1 phase CELL CYCLE regulator.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A broadly expressed type D cyclin. Experiments using KNOCKOUT MICE suggest a role for cyclin D3 in LYMPHOCYTE development.
Product of the retinoblastoma tumor suppressor gene. It is a nuclear phosphoprotein hypothesized to normally act as an inhibitor of cell proliferation. Rb protein is absent in retinoblastoma cell lines. It also has been shown to form complexes with the adenovirus E1A protein, the SV40 T antigen, and the human papilloma virus E7 protein.
Cyclin-dependent kinase 6 associates with CYCLIN D and phosphorylates RETINOBLASTOMA PROTEIN during G1 PHASE of the CELL CYCLE. It helps regulate the transition to S PHASE and its kinase activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P18.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Phase of the CELL CYCLE following G1 and preceding G2 when the entire DNA content of the nucleus is replicated. It is achieved by bidirectional replication at multiple sites along each chromosome.
A cyclin B subtype that colocalizes with MICROTUBULES during INTERPHASE and is transported into the CELL NUCLEUS at the end of the G2 PHASE.
An INK4 cyclin-dependent kinase inhibitor containing five ANKYRIN-LIKE REPEATS. Aberrant expression of this protein has been associated with deregulated EPITHELIAL CELL growth, organ enlargement, and a variety of NEOPLASMS.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
A cyclin D subtype which is regulated by GATA4 TRANSCRIPTION FACTOR. Experiments using KNOCKOUT MICE suggest a role for cyclin D2 in granulosa cell proliferation and gonadal development.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
An E2F transcription factor that interacts directly with RETINOBLASTOMA PROTEIN and CYCLIN A and activates GENETIC TRANSCRIPTION required for CELL CYCLE entry and DNA synthesis. E2F1 is involved in DNA REPAIR and APOPTOSIS.
A cyclin A subtype primarily found in male GERM CELLS. It may play a role in the passage of SPERMATOCYTES into meiosis I.
A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein.
A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include ADENINE and GUANINE, constituents of nucleic acids, as well as many alkaloids such as CAFFEINE and THEOPHYLLINE. Uric acid is the metabolic end product of purine metabolism.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Established cell cultures that have the potential to propagate indefinitely.
A type of CELL NUCLEUS division by means of which the two daughter nuclei normally receive identical complements of the number of CHROMOSOMES of the somatic cells of the species.
A cyclin subtype that is found associated with CYCLIN-DEPENDENT KINASE 5; cyclin G associated kinase, and PROTEIN PHOSPHATASE 2.
The period of the CELL CYCLE following DNA synthesis (S PHASE) and preceding M PHASE (cell division phase). The CHROMOSOMES are tetraploid in this point.
A transcription factor that possesses DNA-binding and E2F-binding domains but lacks a transcriptional activation domain. It is a binding partner for E2F TRANSCRIPTION FACTORS and enhances the DNA binding and transactivation function of the DP-E2F complex.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Nuclear antigen with a role in DNA synthesis, DNA repair, and cell cycle progression. PCNA is required for the coordinated synthesis of both leading and lagging strands at the replication fork during DNA replication. PCNA expression correlates with the proliferation activity of several malignant and non-malignant cell types.
An INK4 cyclin-dependent kinase inhibitor containing four ANKYRIN-LIKE REPEATS. INK4B is often inactivated by deletions, mutations, or hypermethylation in HEMATOLOGIC NEOPLASMS.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
A cyclin G subtype that is constitutively expressed throughout the cell cycle. Cyclin G1 is considered a major transcriptional target of TUMOR SUPPRESSOR PROTEIN P53 and is highly induced in response to DNA damage.
An intracellular signaling system involving the MAP kinase cascades (three-membered protein kinase cascades). Various upstream activators, which act in response to extracellular stimuli, trigger the cascades by activating the first member of a cascade, MAP KINASE KINASE KINASES; (MAPKKKs). Activated MAPKKKs phosphorylate MITOGEN-ACTIVATED PROTEIN KINASE KINASES which in turn phosphorylate the MITOGEN-ACTIVATED PROTEIN KINASES; (MAPKs). The MAPKs then act on various downstream targets to affect gene expression. In mammals, there are several distinct MAP kinase pathways including the ERK (extracellular signal-regulated kinase) pathway, the SAPK/JNK (stress-activated protein kinase/c-jun kinase) pathway, and the p38 kinase pathway. There is some sharing of components among the pathways depending on which stimulus originates activation of the cascade.
A widely-expressed cyclin A subtype that functions during the G1/S and G2/M transitions of the CELL CYCLE.
A family of basic helix-loop-helix transcription factors that control expression of a variety of GENES involved in CELL CYCLE regulation. E2F transcription factors typically form heterodimeric complexes with TRANSCRIPTION FACTOR DP1 or transcription factor DP2, and they have N-terminal DNA binding and dimerization domains. E2F transcription factors can act as mediators of transcriptional repression or transcriptional activation.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Transport proteins that carry specific substances in the blood or across cell membranes.
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Protein kinases that catalyze the PHOSPHORYLATION of TYROSINE residues in proteins with ATP or other nucleotides as phosphate donors.
A CALMODULIN-dependent enzyme that catalyzes the phosphorylation of proteins. This enzyme is also sometimes dependent on CALCIUM. A wide range of proteins can act as acceptor, including VIMENTIN; SYNAPSINS; GLYCOGEN SYNTHASE; MYOSIN LIGHT CHAINS; and the MICROTUBULE-ASSOCIATED PROTEINS. (From Enzyme Nomenclature, 1992, p277)
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
An INK4 cyclin-dependent kinase inhibitor containing five ANKYRIN REPEATS. Aberrant expression of this protein has been associated with TESTICULAR CANCER.
A family of structurally-related proteins that were originally identified by their ability to complex with cyclin proteins (CYCLINS). They share a common domain that binds specifically to F-BOX MOTIFS. They take part in SKP CULLIN F-BOX PROTEIN LIGASES, where they can bind to a variety of F-BOX PROTEINS.
A PROTEIN-TYROSINE KINASE family that was originally identified by homology to the Rous sarcoma virus ONCOGENE PROTEIN PP60(V-SRC). They interact with a variety of cell-surface receptors and participate in intracellular signal transduction pathways. Oncogenic forms of src-family kinases can occur through altered regulation or expression of the endogenous protein and by virally encoded src (v-src) genes.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Proteins and peptides that are involved in SIGNAL TRANSDUCTION within the cell. Included here are peptides and proteins that regulate the activity of TRANSCRIPTION FACTORS and cellular processes in response to signals from CELL SURFACE RECEPTORS. Intracellular signaling peptide and proteins may be part of an enzymatic signaling cascade or act through binding to and modifying the action of other signaling factors.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
A mitogen-activated protein kinase subfamily that regulates a variety of cellular processes including CELL GROWTH PROCESSES; CELL DIFFERENTIATION; APOPTOSIS; and cellular responses to INFLAMMATION. The P38 MAP kinases are regulated by CYTOKINE RECEPTORS and can be activated in response to bacterial pathogens.
Cell lines whose original growing procedure consisted being transferred (T) every 3 days and plated at 300,000 cells per plate (J Cell Biol 17:299-313, 1963). Lines have been developed using several different strains of mice. Tissues are usually fibroblasts derived from mouse embryos but other types and sources have been developed as well. The 3T3 lines are valuable in vitro host systems for oncogenic virus transformation studies, since 3T3 cells possess a high sensitivity to CONTACT INHIBITION.
A superfamily of PROTEIN-SERINE-THREONINE KINASES that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by MITOGEN-ACTIVATED PROTEIN KINASE KINASES, which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP KINASE KINASE KINASES).
A proline-directed serine/threonine protein kinase which mediates signal transduction from the cell surface to the nucleus. Activation of the enzyme by phosphorylation leads to its translocation into the nucleus where it acts upon specific transcription factors. p40 MAPK and p41 MAPK are isoforms.
A serine-threonine protein kinase family whose members are components in protein kinase cascades activated by diverse stimuli. These MAPK kinases phosphorylate MITOGEN-ACTIVATED PROTEIN KINASES and are themselves phosphorylated by MAP KINASE KINASE KINASES. JNK kinases (also known as SAPK kinases) are a subfamily.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (CYTOSINE; THYMINE; and URACIL) and form the basic structure of the barbiturates.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Elements of limited time intervals, contributing to particular results or situations.
A group of enzymes that are dependent on CYCLIC AMP and catalyze the phosphorylation of SERINE or THREONINE residues on proteins. Included under this category are two cyclic-AMP-dependent protein kinase subtypes, each of which is defined by its subunit composition.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
A 44-kDa extracellular signal-regulated MAP kinase that may play a role the initiation and regulation of MEIOSIS; MITOSIS; and postmitotic functions in differentiated cells. It phosphorylates a number of TRANSCRIPTION FACTORS; and MICROTUBULE-ASSOCIATED PROTEINS.
A protein-serine-threonine kinase that is activated by PHOSPHORYLATION in response to GROWTH FACTORS or INSULIN. It plays a major role in cell metabolism, growth, and survival as a core component of SIGNAL TRANSDUCTION. Three isoforms have been described in mammalian cells.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
BENZOIC ACID amides.
The rate dynamics in chemical or physical systems.
A subgroup of mitogen-activated protein kinases that activate TRANSCRIPTION FACTOR AP-1 via the phosphorylation of C-JUN PROTEINS. They are components of intracellular signaling pathways that regulate CELL PROLIFERATION; APOPTOSIS; and CELL DIFFERENTIATION.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A cyclin B subtype that colocalizes with GOLGI APPARATUS during INTERPHASE and is transported into the CELL NUCLEUS at the end of the G2 PHASE.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
A group of phenyl benzopyrans named for having structures like FLAVONES.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Recent studies suggest that ANRIL expression mediates susceptibility to CAD1 via CDKN2B.2 We used fluorescently-labelled whole-blood RNA, from 20 healthy volunteers genotyped for the CAD-risk-SNP rs2891168, to probe custom-designed Agilent tiling expression microarrays. Raw data were normalized to probe GC content and housekeeping genes. We found that ANRIL exons 1-4 were more abundantly expressed in blood than 5-20, with exons 6, 8, 9, 20 showing low expression. We derived a set of training tiling probes from HUVEC cells in which ANRIL expression was attenuated using siRNA against exons 13 and 19. ANRIL expression (probes in exons 5,6,8,13,16,18,19) was reduced by at least 50% and CDKN2B expression (probes in exons 1,2) increased, with no effect on CDKN2A. We confirmed these data using real-time QPCR. Using the tiling probe training-set, a probe in exon 16 of ANRIL showed a CAD genotype-specific difference in expression (p,0.001), with the risk-allele lower, and probes in exon 2 of CDKN2B ...
Results In the global gene expression analysis, we found strong cis eQTLs for both CDKN2B (p=1.3×10−38) and MTAP (p=6.6×10−23), explaining 17.0% and 8.0% of the expression of these genes. AE analysis confirmed these findings (CDKN2B, p=6.0×10−64; MTAP, p=1.4×10−38) and also showed a significant cis-eQTL effect on ANRIL expression (p=3.5×10−28). Interestingly, the SNPs associated with CDKN2B and ANRIL expression were the same. However, the SNPs showing e-QTL effects were distinct from SNPs that showed an association with CAD risk (p=2.2×10−12). Even in the region with a physical overlap of variants affecting expression of CDKN2B/ANRIL and CAD risk, the effects of the respective variants were independent of each other. Expression of CDKN2A and ARF was low but did not show any obvious eQTL effect, or differences according to genotype at CAD-associated SNPs. ...
Patients with ALL can have abnormalities of chromosome number as well as balanced translocations Patients with a normal karyotype and those with isolated 9p/CDKN2A-CDKN2B deletions have had a relativ... more
Hepatocellular carcinoma (HCC) is a common malignant tumor with high fatality rate. Recent studies reported that up-regulation of long non-coding RNA antisense non-coding RNA in the INK4 locus (lncRNA ANRIL) was found in HCC tissues, and which could affect HCC cells biological processes. However, the potential molecular mechanism of ANRIL in HCC is still unclear. The study aimed to uncover the effect of ANRIL on HepG2 cells growth, migration and invasion. The knockdown expression vectors of ANRIL were transfected into HepG2 cells, and qRT-PCR, CCK-8, flow cytometry, Transwell and western blot assays were performed to analyze the effect of ANRIL on cell proliferation, apoptosis, migration and invasion. The relative expression of miR-191 was then examined in ANRIL knockdown vector transfected cells. These experiments were repeated again for exploring the effect of miR-191 on HepG2 cells. NF-κB and Wnt/β-catenin signaling pathways were examined by using western blot assay. Knockdown of ANRIL inhibited
TY - JOUR. T1 - Restricted heterochromatin formation links NFATc2 repressor activity with growth promotion in pancreatic cancer. AU - Baumgart, Sandra. AU - Glesel, Elisabeth. AU - Singh, Garima. AU - Chen, Naiming. AU - Reutlinger, Kristina. AU - Zhang, Jinsan. AU - Billadeau, Daniel D. AU - Fernandez-Zapico, Martin E. AU - Gress, Thomas M.. AU - Singh, Shiv K.. AU - Ellenrieder, Volker. PY - 2012/2. Y1 - 2012/2. N2 - Background & Aims: Transcriptional silencing of the p15 INK4b tumor suppressor pathway overcomes cellular protection against unrestrained proliferation in cancer. Here we show a novel pathway involving the oncogenic transcription factor nuclear factor of activated T cells (NFAT) c2 targeting a p15 INK4b-mediated failsafe mechanism to promote pancreatic cancer tumor growth. Methods: Immunohistochemistry, real-time polymerase chain reaction, immunoblotting, and immunofluorescence microscopy were used for expression studies. Cancer growth was assessed in vitro by [ 3H] thymidine ...
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My laboratory studies the mechanisms through which Polycomb group proteins regulate the INK4a-ARF-INK4b tumour suppressor locus, the most frequent site of genetic alterations in human cancer. The three gene products are each capable of bringing cell proliferation to a halt and their primary role appears to be the implementation of senescence, the state of permanent cell cycle arrest elicited by various forms of stress.. Keywords: Senescence / tumour suppressors / INK4a/ARF / Polycomb complexes. Subject area(s): Chromatin & Transcription , Differentiation & Death , Molecular Medicine. ...
TY - JOUR. T1 - Tumor suppressor ASXL1 is essential for the activation of INK4B expression in response to oncogene activity and anti-proliferative signals. AU - Wu, Xudong. AU - Bekker-Jensen, Ida Holst. AU - Christensen, Jesper. AU - Rasmussen, Kasper Dindler. AU - Sidoli, Simone. AU - Qi, Yan. AU - Kong, Yu. AU - Wang, Xi. AU - Cui, Yajuan. AU - Xiao, Zhijian. AU - Xu, Guogang. AU - Williams, Kristine. AU - Rappsilber, Juri. AU - Sønderby, Casper Kaae. AU - Winther, Ole. AU - Jensen, Ole N.. AU - Helin, Kristian. PY - 2015. Y1 - 2015. N2 - ASXL1 mutations are frequently found in hematological tumors, and loss of Asxl1 promotes myeloid transformation in mice. Here we present data supporting a role for an ASXL1-BAP1 complex in the deubiquitylation of mono-ubiquitylated lysine 119 on Histone H2A (H2AK119ub1) in vivo. The Polycomb group proteins control the expression of the INK4B-ARF-INK4A locus during normal development, in part through catalyzing mono-ubiquitylation of H2AK119. Since the ...
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References for Abcams Human CDKN2A/p16INK4a peptide (ab105631). Please let us know if you have used this product in your publication
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CDKN2B-AS, also known as ANRIL (antisense non-coding RNA in the INK4 locus) is a long non-coding RNA consisting of 19 exons, spanning 126.3kb in the genome, and its spliced product is a 3834bp RNA. It is located within the p15/CDKN2B-p16/CDKN2A-p14/ARF gene cluster, in the antisense direction. Single nucleotide polymorphisms (SNPs) which alter the expression of CDKN2B-AS are associated with many diseases, including coronary artery disease, diabetes and many cancers. It binds to chromobox 7 (CBX7) within the polycomb repressive complex 1 and to SUZ12, a component of polycomb repression complex 2 and through these interactions is involved in transcriptional repression. Long noncoding RNA GRCh38: Ensembl release 89: ENSG00000240498 - Ensembl, May 2017 Human PubMed Reference:. Cunnington MS, Santibanez Koref M, Mayosi BM, Burn J, Keavney B (2010). Gibson G, ed. Chromosome 9p21 SNPs Associated with Multiple Disease Phenotypes Correlate with ANRIL Expression. PLoS Genet. 6 (4): e1000899. ...
DB-ID: Database ID of variant, grouping multiple observations of the same variant together, starting with the HGNC gene symbol, followed by an underscore (_) and a six digit number (e.g. DMD_012345). _000000 is used for variants where DNA was not analysed (change predicted from RNA analysis), variants seen in animal models or variants not seen in humans but functionally tested in vitro ...
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The function of the squids ink sac is to keep it protected from predators.The ink sac squirts out bursts of ink that allow the squid ample time to escape the...
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CDKN2A; ARF; CDK4I; CDKN2; CMM2; INK4; INK4A; MLM; MTS-1; MTS1; P14; P14ARF; P16; P16-INK4A; P16INK4; P16INK4A; P19; P19ARF; TP16 ...
An aqueous ink comprising at least one dye having at least one ionic hydrophilic group within a molecule thereof and represented by the following formula (1): ##STR00001## wherein A and B each indepen
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A printhead chip for an ink jet printhead includes a substrate. A plurality of nozzle arrangements is positioned on the substrate. Each nozzle arrangement has an active ink ejection structure that is positioned on the substrate and spaced from the substrate. The active ink ejection structure has a roof with an ink ejection port defined in the roof. A static ink ejection structure is positioned on the substrate. The active ink ejection structure and the static ink ejection structure together define a nozzle chamber in fluid communication with an ink supply. The active ink ejection structure is displaceable with respect to the static ink ejection structure towards and away from the substrate to reduce and increase a volume of the nozzle chamber to eject an ink drop from the nozzle chamber. At least two actuators are operatively arranged with respect to the active ink ejection structure to displace the active ink ejection structure with respect to the static ink ejection structure towards and away from the
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By applying 21st century, state-of-the-art technology to reveal the hidden secrets of ancient ink technology, we are contributing to the unveiling the origin of writing practices., explains Marine Cotte, scientist at the ESRF and co-corresponding author of the paper.. Something very striking was that we found that lead was added to the ink mixture, not as a dye, but as a dryer of the ink, so that the ink would stay on the papyrus, says Cotte. The researchers came to this conclusion because they did not find any other type of lead, like lead white or minium, which should be present if lead was used as a pigment. The fact that the lead was not added as a pigment but as a dryer infers that the ink had quite a complex recipe and could not be made by just anyone. We hypothesise that there were workshops specialised in preparing inks, adds Thomas Christiansen, Egyptologist from the University of Copenhagen and co-corresponding author of the paper. A surprising fact is that the ink recipe can be ...
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Combined effects of increasing numbers of the risk alleles from CDKAL1-rs9465871, CDKN2A/B-rs10811661, IGF2BP2-rs4402960, and SLC30A8-rs13266634. A: The risk al
... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4))". Atlas of genetics and cytogenetics in oncology and haematology. ... INK4 is a family of cyclin-dependent kinase inhibitors (CKIs). The members of this family (p16INK4a, p15INK4b, p18INK4c, ... Ortega S, Malumbres M, Barbacid M (March 2002). "Cyclin D-dependent kinases, INK4 inhibitors and cancer". Biochimica et ... p19INK4d) are inhibitors of CDK4 (hence their name INhibitors of CDK4), and of CDK6. The other family of CKIs, CIP/KIP proteins ...
"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... "Entrez Gene: CDKN2B cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4)". Tu Q, Hao J, Zhou X, Yan L, Dai H, Sun B, et al ... an alternatively spliced form of p15 cyclin-dependent kinase inhibitor". Cancer Research. 57 (14): 2966-73. PMID 9230210. Rich ... Cyclin-dependent kinase 4 inhibitor B also known as multiple tumor suppressor 2 (MTS-2) or p15INK4b is a protein that is ...
"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... CDK4, CMM3, PSK-J3, cyclin-dependent kinase 4, cyclin dependent kinase 4. ... See also CDK inhibitor for inhibitors of various CDKs. Interactions[edit]. Cyclin-dependent kinase 4 has been shown to interact ... protein kinase activity. • kinase activity. • protein serine/threonine kinase activity. • cyclin-dependent protein serine/ ...
"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... Cyclins function as activating subunits of enzymatic complex together with cyclin-dependent kinases (CDKs). Different cyclins ... and the Kip/Cip family of CDK-inhibitor proteins. Cyclin-A1 interacts with: CDC20, Cyclin-dependent kinase 2, E2F1, GNB2L1, ... cyclins and cyclin dependent kinases". Oncogene. 15 (2): 143-157. doi:10.1038/sj.onc.1201252. PMID 9244350. Suzuki Y, Yoshitomo ...
Inactivation of cyclin D is triggered by several cyclin-dependent kinase inhibitor protein (CKIs) like the INK4 family (e.g. ... p14, p15, p16, p18). INK4 proteins are activated in response to hyperproliferative stress response that inhibits cell ... activate cyclin D gene in response to integrin. p27kip1 and p21cip1 are cyclin-dependent kinase inhibitors (CKIs) which ... Cyclins are eukaryotic proteins that form holoenzymes with cyclin-dependent protein kinases (Cdk), which they activate. The ...
"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... Hall M, Peters G (1996). Genetic alterations of cyclins, cyclin-dependent kinases, and Cdk inhibitors in human cancer. Advances ... Cyclins function as regulators of CDKs (Cyclin-dependent kinase). Different cyclins exhibit distinct expression and degradation ... cyclin box domain for cyclin-dependent kinase (CDK) binding and CDK inhibitor binding; LxxLL binding motif for co-activator ...
"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... "Entrez Gene: CDK4 cyclin-dependent kinase 4". "CDK4 - Cyclin-dependent kinase 4 - Homo sapiens (Human) - CDK4 gene & protein". ... See also CDK inhibitor for inhibitors of various CDKs. Cyclin-dependent kinase 4 has been shown to interact with: CDC37, CDKN1B ... 1995). "Identification of human cyclin-dependent kinase 8, a putative protein kinase partner for cyclin C". Proc. Natl. Acad. ...
They are p15, p16, p18, p19, p21, p27, and p57. Russo AA, Jeffrey PD, Patten AK, Massagué J, Pavletich NP (July 1996). "Crystal ... A cyclin-dependent kinase inhibitor protein is a protein which inhibits the enzyme cyclin-dependent kinase (CDK). Several ... Seven cyclin-dependent kinase inhibitor proteins have thus far been identified. They are named by the small letter "p" followed ... Cyclin-Dependent+Kinase+Inhibitor+Proteins at the US National Library of Medicine Medical Subject Headings (MeSH) v t e. ...
Furthermore, inhibitors of the INK4 family members like p15, p16, p18 and p19 inhibit the monomer of CDK6, preventing the ... Cyclin D1, Cyclin D3, P16, PPM1B, and PPP2CA. Cell cycle Cyclin-dependent kinase Cyclin-dependent kinase 4 Mitosis The ... "Both p16 and p21 families of cyclin-dependent kinase (CDK) inhibitors block the phosphorylation of cyclin-dependent kinases by ... It is regulated by cyclins, more specifically by Cyclin D proteins and Cyclin-dependent kinase inhibitor proteins. The protein ...
CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... "Identification of human cyclin-dependent kinase 8, a putative protein kinase partner for cyclin C". Proceedings of the National ... protein serine/threonine kinase activity. • cyclin-dependent protein serine/threonine kinase activity. ... The protein encoded by this gene is a member of the cyclin-dependent protein kinase (CDK) family. CDK8 and cyclin C associate ...
"CDKN2A cyclin dependent kinase inhibitor 2A [Homo sapiens (human)] - Gene - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2016-10-11. ... Kanellou P, Zaravinos A, Zioga M, Spandidos DA (June 2009). "Deregulation of the tumour suppressor genes p14(ARF), p15(INK4b), ... CDKN2A, also known as cyclin-dependent kinase inhibitor 2A, is a gene which in humans is located at chromosome 9, band p21.3. ... "CDKN2A - Cyclin-dependent kinase inhibitor 2A - Homo sapiens (Human) - CDKN2A gene & protein". www.uniprot.org. Retrieved 2016- ...
... and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21". J. Biol. Chem. ... Yu P, Huang B, Shen M, Lau C, Chan E, Michel J, Xiong Y, Payan DG, Luo Y (Jan 2001). "p15(PAF), a novel PCNA associated factor ... and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21". J. Biol. Chem. ... Henneke G, Koundrioukoff S, Hübscher U (Jul 2003). "Phosphorylation of human Fen1 by cyclin-dependent kinase modulates its role ...
... cyclin-dependent kinase inhibitor 1A, cyclin dependent kinase inhibitor 1A. External IDs. OMIM: 116899 MGI: 104556 HomoloGene: ... Yu P, Huang B, Shen M, Lau C, Chan E, Michel J, Xiong Y, Payan DG, Luo Y (January 2001). "p15(PAF), a novel PCNA associated ... also known as cyclin-dependent kinase inhibitor 1 or CDK-interacting protein 1, is a cyclin-dependent kinase inhibitor (CKI) ... cyclin binding. • cyclin-dependent protein kinase activating kinase activity. • cyclin-dependent protein serine/threonine ...
Cyclin D1, Cyclin O, Cyclin-dependent kinase 4, Cyclin-dependent kinase inhibitor 1C, DNMT1, EP300, Establishment of Sister ... Yu P, Huang B, Shen M, Lau C, Chan E, Michel J, Xiong Y, Payan DG, Luo Y (January 2001). "p15(PAF), a novel PCNA associated ... "A small peptide inhibitor of DNA replication defines the site of interaction between the cyclin-dependent kinase inhibitor ... and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21". J. Biol. Chem. ...
CDK抑制因子(英语:Cyclin-dependent kinase inhibitor protein). *INK4a/ARF(p14arf/p16、p15、p18、p19) ... Cyclin-dependent protein kinases: key regulators of the eukaryotic cell cycle. BioEssays. June 1995, 17 (6): 471-80. PMID ... 細胞週期的進行是由不同的週期素(Cyclin)所調控。週期素意味著這些蛋白質的表現量會隨著細胞週期的進行而有所變化,進而確認週期素原來是扮演細胞
... inducing expression of cyclin-dependent kinase inhibitor 21 (a regulator of cell cycle progression through the G1 and S phase ... TGF-β causes synthesis of p15 and p21 proteins, which block the cyclin:CDK complex responsible for retinoblastoma protein (Rb) ... SB-431542 is a potent and specific inhibitor of transforming growth factor-beta superfamily type I activin receptor-like kinase ... After the binding of TGF-β, the type 2 receptor kinase phosphorylates and activates the type 1 receptor kinase that activates a ...
The cell cycle is regulated by complex network of cyclins, cyclin-dependent kinases (Cdk), cyclin-dependent kinase inhibitors ( ... Furthermore, regulators of Cdk4 and Cdk6 activity, such as members of the Ink family of inhibitors (p15, p16, p18, and p19), ... hESCs show that the activities of Cyclin E/Cdk2 and Cyclin A/Cdk2 complexes are cell cycle-dependent and the Rb checkpoint in ... However, in mESCs, this typically ordered and oscillatory activity of Cyclin-Cdk complexes is absent. Rather, the Cyclin E/Cdk2 ...
Li Y, Jenkins CW, Nichols MA, Xiong Y. Cell cycle expression and p53 regulation of the cyclin-dependent kinase inhibitor p21. „ ... Yu P, Huang B, Shen M, Lau C, Chan E, Michel J, Xiong Y, Payan DG, Luo Y. p15(PAF), a novel PCNA associated factor with ... The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases. „Cell". 75 (4), s. 805-816, 1993. ... a b Entrez Gene: CDKN1A cyclin-dependent kinase inhibitor 1A (p21, Cip1). ...
September 2009). "Nuclear targeting of 6-phosphofructo-2-kinase (PFKFB3) increases proliferation via cyclin-dependent kinases ... April 2015). "Structure-Based Design of Potent and Selective Inhibitors of the Metabolic Kinase PFKFB3". Journal of Medicinal ... "The third human isoform of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3) map position 10p14-p15". Chromosome ... and suppresses apoptosis by regulating cyclin-dependent kinase 1 (Cdk-1). PFKFB3's synthesis of F2,6BP in the nucleus was found ...
... cyclin-dependent kinase inhibitor p15 MeSH D12.776.624.776.355.200 - cyclin-dependent kinase inhibitor p16 MeSH D12.776.624.776 ... cyclin-dependent kinase inhibitor p27 MeSH D12.776.624.776.355.700 - cyclin-dependent kinase inhibitor p57 See List of MeSH ... cyclin-dependent kinase inhibitor p18 MeSH D12.776.624.776.355.400 - cyclin-dependent kinase inhibitor p19 MeSH D12.776.624.776 ... cyclin-dependent kinase 5 MeSH D12.776.167.200.067.900 - cyclin-dependent kinase 9 MeSH D12.776.167.200.580.500 - cdc2 protein ...
Yik JH, Chen R, Nishimura R, Jennings JL, Link AJ, Zhou Q (October 2003). "Inhibition of P-TEFb (CDK9/Cyclin T) kinase and RNA ... The existence of an RNAP III-dependent ncRNA transcriptome that regulates its RNAP II-dependent counterpart was supported by a ... was able to induce changes to heterochromatin and DNA methylation status of p15 by an unknown mechanism, thereby regulating p15 ... Liu WM, Chu WM, Choudary PV, Schmid CW (May 1995). "Cell stress and translational inhibitors transiently increase the abundance ...
The cyclin-dependent kinase inhibitor SCH 727965 (dinacliclib) induces the apoptosis of osteosarcoma cells. „Mol Cancer Ther". ... Stwierdzono także mutacje genów supresorowych p16 (CDKN2A), p14 (ARF) i p15 (CDKN2B) wpływających na inaktywację CDK[103][75]. ... Glycogen synthase kinase-3β, NF-κB signaling, and tumorigenesis of human osteosarcoma. „J Natl Cancer Inst". 104 (10), s. 749- ... GSK-3 inhibitor inhibits cell proliferation and induces apoptosis in human osteosarcoma cells. „Oncol Rep". 35 (4), s. 2348-54 ...
... *Cyclin-dependent kinase inhibitor protein. *Cyclin-dependent kinase. *Cyclin. Lipid. *Phosphoinositide phospholipase C ... CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... cyclin E, A (Cdk2,1) cyclin A, B, B3 (Cdk1) H. sapiens cyclin D 1,2,3 (Cdk4, Cdk6) cyclin E (Cdk2) cyclin A (Cdk2, Cdk1) cyclin ... Cyclin A / CDK2 - active in S phase.. *Cyclin D / CDK4, Cyclin D / CDK6, and Cyclin E / CDK2 - regulates transition from G1 to ...
All these phases in the cell cycle are highly regulated by cyclins, cyclin-dependent kinases, and other cell cycle proteins. ... CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... Generation of pressure is dependent on formin-mediated F-actin nucleation[71] and Rho kinase (ROCK)-mediated myosin II ... This can occur when cells become overcrowded (density-dependent inhibition) or when they differentiate to carry out specific ...
CDK-activating kinase. CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19) ... Caspases are proteins that are highly conserved, cysteine-dependent aspartate-specific proteases. There are two types of ... Cyclin. *A (A1, A2). *B (B1, B2, B3). *D (D1, D2, D3) ... Using these inhibitors it was discovered that cells can die ... The characterization of the caspases allowed the development of caspase inhibitors, which can be used to determine whether a ...
CDK-activating kinase. CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19) ... April 2010). "Apoptosis induced by Oropouche virus infection in HeLa cells is dependent on virus protein expression". Virus Res ... Cyclin. *A (A1, A2). *B (B1, B2, B3). *D (D1, D2, D3) ... Using these inhibitors it was discovered that cells can die ... The characterization of the caspases allowed the development of caspase inhibitors, which can be used to determine whether a ...
Expression of Myc is highly dependent on BRD4 function in some cancers.[22][23] BET inhibitors have been used to successfully ... "Mitogen-activated protein kinase kinase 7 is an activator of the c-Jun NH2-terminal kinase". Proceedings of the National ... "Direct interaction of c-Myc with Smad2 and Smad3 to inhibit TGF-beta-mediated induction of the CDK inhibitor p15(Ink4B)". ... The first to be discovered was its capability to drive cell proliferation (upregulates cyclins, downregulates p21), but it also ...
Expression of Myc is highly dependent on BRD4 function in some cancers. BET inhibitors have been used to successfully block Myc ... "Mitogen-activated protein kinase kinase 7 is an activator of the c-Jun NH2-terminal kinase". Proceedings of the National ... "Direct interaction of c-Myc with Smad2 and Smad3 to inhibit TGF-beta-mediated induction of the CDK inhibitor p15(Ink4B)". ... Myc has been shown to interact with: ACTL6A BRCA1 Bcl-2 Cyclin T1 CHD8 DNMT3A EP400 GTF2I HTATIP let-7 MAPK1 MAPK8 MAX MLH1 ...
CDK-activating kinase. CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19) ... Cyclin. *A (A1, A2). *B (B1, B2, B3). *D (D1, D2, D3) ... cAMP-dependent pathway. *Ca2+ signaling. *Lipid signaling. ... "Predominant suppression of apoptosome by inhibitor of apoptosis protein in non-small cell lung cancer H460 cells: therapeutic ...
CDK-activating kinase. CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19) ... GTP-dependent protein binding. • GTPase activity. • mitogen-activated protein kinase kinase kinase binding. • protein binding. ... Cyclin. *A (A1, A2). *B (B1, B2, B3). *D (D1, D2, D3) ... "The MAP kinase kinase kinase MLK2 co-localizes with activated ... protein kinase binding. • nucleotide binding. • GTP binding. • identical protein binding. Cellular component. • cytoplasm. • ...
... a cyclin dependent kinase (CDK), and a cyclin dependent kinase inhibitor (CDKI). The progression of cells through the cell ... cyclin-dependent kinases (CDKs), growth suppressor genes and cyclin-dependent kinase inhibitors (CKIs). Oncogene. 1995, 11: 211 ... The expression of cyclin-dependent kinase inhibitors p15, p16, p21, and p27 during ovarian follicle growth initiation in the ... Cyclin-dependent kinase inhibitors (CDKIs) are proteins that bind to and inhibit the activity of CDKs. Two major classes of CDK ...
Deletion of the p15-p14-p16 genomic locus could be one of the molecular aberrations in canine lymphoid tumor cells. ... Two of the six canine lymphoid tumor cell lines did not express detectable levels of p16, p15 and p14 mRNAs, and wide-ranging ... Based on the sequence data, primers specific for p16, p15 and p14 were designed. Using these primers, the expression of p16, ... p15 and p14 mRNAs could be individually evaluated by reverse transcriptase polymerase chain reaction. Genomic aberrations were ...
... is a potent T cell inhibitor with a critical role in peripheral tolerance, but it can also compromise anti-viral and antitumor ... Cyclin-Dependent Kinase 2 / metabolism * Cyclin-Dependent Kinase Inhibitor p15 / metabolism* * Cyclin-Dependent Kinase ... PD-1 did not alter the expression of G 1 phase cyclins or cyclin-dependent kinases (Cdks) but, instead, suppressed the ... These events resulted in upregulation of the Cdk4/6 inhibitor p15 (INK4B) and repression of the Cdk-activating phosphatase ...
Cyclin-Dependent Kinase Inhibitor p15 / genetics * DNA Helicases / genetics * Female * Genome-Wide Association Study ...
... anti-cyclin D, anti-p27Kip1, anti-p21CIP1, or anti-p15INK4b. Protein bands were detected using the Amersham ECL kit with ... cyclins and cyclin-dependent kinase inhibitors (cdkis) known to regulate cell cycle progression through this phase are affected ... 1997) Accumulation of the cyclin-dependent kinase inhibitor p27/Kip1 and the timing of oligodendrocyte differentiation. EMBO J ... Blockage of K+ channels and membrane depolarization also caused accumulation of the cyclin-dependent kinase inhibitors p27Kip1 ...
1995) Transforming growth factor β activates the promoter of cyclin-dependent kinase inhibitor p15INK4B through an Sp1 ... and TGF-β activates cyclin-dependent kinase inhibitor p15INK4B (Li et al., 1995; Collazo et al., 1992) and α2(I) collagen gene ... two are for cyclin-dependent protein kinase (CDK) (Ser/Thr-ProX-Lys/Arg) (Moodie et al., 1993), and one is for glycogen ... 1993) Complex of ras-GTP with raf1 and mitogen-activated protein kinase kinase. Science 260:1658-1661. ...
Koduru PR, Zariwala M, Soni M, Gong JZ, Xiong Y, Broome JD . Deletion of cyclin-dependent kinase 4 inhibitor genes P15 and P16 ... including the gene encoding the cyclin-dependent kinase inhibitor p15INK4b, the interferon gene cluster, and the ... Gombart AF, Morosetti R, Miller CW, Said JW, Koeffler HP . Deletions of the cyclin-dependent kinase inhibitor genes p16INK4A ... The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases Cell 1993 75: 805-816 ...
Cyclin Dependent Kinase Inhibitor 2B, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards ... cyclin dependent kinases 4 and 6 (CDK4/CDK6) inhibitor,p15,regulator of cell cycle,passage through the G1 checkpoint,tightly ... Cyclin-dependent kinase 4 inhibitor B Protein Accession:. P42772. Secondary Accessions: *O15125 ... CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) is a Protein Coding gene. Diseases associated with CDKN2B include Scrotal ...
... a cyclin-dependent kinase inhibitor ... ... The expression of p15(INK4b), ... Cytochrome P450 (CYP)-dependent eicosanoids regulate vascular function, inflammation, and angiogenesis, which are ... The outcomes of ecologically more relevant ramping experiments, however, are dependent on the rate of temperature change ... Plaque-Stabilizing Effect of Angiotensin-Converting Enzyme Inhibitor and/or Angiotensin Receptor Blocker in a ... ...
The gene codes for a protein, p15, which is an inhibitor of cyclin dependent kinases, and thus, acts as a negative regulator of ... p15 interacts strongly with cyclin-dependent kinases CDK4 and CDK6, and inhibits their ability to interact with cyclins D, ... P15 gene deletions were examined by polymerase chain reaction (PCR). In all normal samples, p15 gene was detected. P15 gene was ... Deletion of the p15 gene was observed in 36 bladder tumors. The expression of p15 protein was undetectable in 38 bladder tumors ...
P15; MTS2; INK4B; TP15; CDK4I; p15INK4b Common name. cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) Potential ... cyclin-dependent protein serine/threonine kinase inhibitor activity. GO:0005515; protein binding. GO:0019901; protein kinase ... GO:0000079; regulation of cyclin-dependent protein serine/threonine kinase activity. GO:0000086; G2/M transition of mitotic ... The p15 tumor suppressor (CDKN2B) is located in the same region as p16 (CDKN2A), and is also involved in cell cycle, senescence ...
Cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4). NM_078487. NM_004936. Gene Info. ... Cyclin-dependent kinase inhibitor 1C (p57, Kip2). NM_000076. NM_001122630. NM_001122631. Gene Info. ... Cyclin-dependent kinase inhibitor 2A. NM_001195132. NM_000077. NM_058197. NM_058195. Gene Info. ... Cyclin-dependent kinase 1. NM_001786. NM_001170406. NM_033379. NM_001170407. Gene Info. ...
... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4))". Atlas of genetics and cytogenetics in oncology and haematology. ... INK4 is a family of cyclin-dependent kinase inhibitors (CKIs). The members of this family (p16INK4a, p15INK4b, p18INK4c, ... Ortega S, Malumbres M, Barbacid M (March 2002). "Cyclin D-dependent kinases, INK4 inhibitors and cancer". Biochimica et ... p19INK4d) are inhibitors of CDK4 (hence their name INhibitors of CDK4), and of CDK6. The other family of CKIs, CIP/KIP proteins ...
p15, a target of transforming growth factor-β signaling,16 is an inhibitor of the cyclin-dependent kinase-417 18 and a negative ... p16 and p15, 2 inhibitors of cyclin-dependent kinases, are frequently hypermethylated in hematologic neoplasias. Decitabine, or ... Review of alterations of cyclin-dependent kinase inhibitor INK4 family genes p15, p16, p18 and p19 in human leukemia-lymphoma ... Inactivation of the cyclin-dependent kinase inhibitor p15INK4b by deletion and de novo methylation with independence of ...
They are p15, p16, p18, p19, p21, p27, and p57. Russo AA, Jeffrey PD, Patten AK, Massagué J, Pavletich NP (July 1996). "Crystal ... A cyclin-dependent kinase inhibitor protein is a protein which inhibits the enzyme cyclin-dependent kinase (CDK). Several ... Seven cyclin-dependent kinase inhibitor proteins have thus far been identified. They are named by the small letter "p" followed ... Cyclin-Dependent+Kinase+Inhibitor+Proteins at the US National Library of Medicine Medical Subject Headings (MeSH) v t e. ...
... cyclin-dependent kinase inhibitor 2B) for WB. Anti-p15 INK4b pAb (GTX77673) is tested in Human samples. 100% Ab-Assurance. ... cyclin-dependent kinase inhibitor 2B. Background. This gene lies adjacent to the tumor suppressor gene CDKN2A in a region that ... This gene encodes a cyclin-dependent kinase inhibitor, which forms a complex with CDK4 or CDK6, and prevents the activation of ... TP15 Antibody , INK4B Antibody , CDKN2B Antibody , CDK4I Antibody , MTS2 Antibody , P15 Antibody , P15INK4B Antibody. ...
An upregulation of the cyclin-dependent kinase inhibitor p15 and of the proapoptotic protein Bim can be observed. There is ... Based on a screen of various kinase inhibitors, p38MAPK and Janus kinase were identified to mediate Nrf2 phosphorylation/ ... ARE-dependent genes are involved in the removal of ROI, that is, glutathione-dependent peroxidase (GPx), in the glutathione ... AMP-activated protein kinase inhibits the mTOR kinase activity, causing an activation of autophagy [105]. This canonical ...
Cloning and Characterization of p10, an Alternatively Spliced Form of p15 Cyclindependent Kinase Inhibitor ... Cyclin-dependent Kinase 6 Is the Principal Target of p27/Kip1 Regulation of the G1-phase Traverse in 1,25-Dihydroxyvitamin D3- ... Cloning and Characterization of p10, an Alternatively Spliced Form of p15 Cyclindependent Kinase Inhibitor ... Cloning and Characterization of p10, an Alternatively Spliced Form of p15 Cyclindependent Kinase Inhibitor ...
CDKN2B (cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4)). CREATED 2011-01 Lab Cell Oncology, National Cancer ... MAPKAPK2 (mitogen-activated protein kinase-activated protein kinase 2). CREATED 2010-04 Laboratory of Cancer Molecular Biology ... VRK2 (vaccinia related kinase 2). CREATED 2012-05 Instituto de Biologia Molecular y Celular del Cancer, CSIC-Universidad de ... KSR1 (kinase suppressor of ras 1). CREATED 2011-02 Eppley Institute for Cancer Research, University of Nebraska Medical Center ...
"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... CDK4, CMM3, PSK-J3, cyclin-dependent kinase 4, cyclin dependent kinase 4. ... See also CDK inhibitor for inhibitors of various CDKs. Interactions[edit]. Cyclin-dependent kinase 4 has been shown to interact ... protein kinase activity. • kinase activity. • protein serine/threonine kinase activity. • cyclin-dependent protein serine/ ...
INK4 represents a family of cyclin-dependent kinase inhibitors. This gene encodes several proteins that are often targeted ... early during malignant progression, including p14, p15, and p16. Histone modification is another epigenetically important ... 2013). Modulation of Nrf2-dependent gene transcription by bilberry anthocyanins in vivo. Mol. Nutr. Food Res. 57, 545-550. doi ... It is an inhibitor of the Histone acetlytransferase p300/CBP (co-activator) and GATA4 (a zinc finger transcription factor), ...
... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4)) for ICC/IF, IP. Anti-p15 INK4b mAb (GTX72279) is tested in Human ... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4). Background. p15INK4b is a specific inhibitor of cdk4/cdk6 and is ... Storage Conditions: p15 INK4b antibody [DCS-114]. Storage Buffer. 10mM Phosphate-buffered saline containing 0.2% BSA and 0.1% ... For IF: Use at an assay dependent dilution. For IP: (Native verified) Use Protein G. Use at a dilution of 1:400. Not suitable ...
CDK4I,INK4B,MTS2,P15,TP15,p15INK4b. *Gene Description:. *cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) ... cyclin-dependent kinase 4 inhibitor B,cyclin-dependent kinase inhibitor 2B,cyclin-dependent kinases 4 and 6 binding protein, ... Inhibitors of mammalian G1 cyclin-dependent kinases.. Sherr CJ, Roberts JM.Genes Dev. 1995 May 15;9(10):1149-63. ... This gene encodes a cyclin-dependent kinase inhibitor, which forms a complex with CDK4 or CDK6, and prevents the activation of ...
cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) Assay Type: Probe Assay Design: exonic Application: Gene Expression ... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) Assay Type: SYBR® Green Assay Design: Exonic Application: Gene ... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) Assay Type: SYBR® Green Assay Design: exonic Application: Gene ... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) Assay Type: EvaGreen Application: Gene Expression Unique Assay ID: ...
Transforming growth factor β activates the promoter of cyclin-dependent kinase inhibitor P15INK4B through a Sp1 consensus site ... Bach2 Promotes B Cell Receptor-Induced Proliferation of B Lymphocytes and Represses Cyclin-Dependent Kinase Inhibitors ... Identification of regulatory sequences in the type I plasminogen activator inhibitor gene responsive to TGFβ. J. Biol. Chem. ... Assembly and function of a TCRα enhancer complex is dependent on LEF-1-induced DNA bending and multiple protein-protein ...
Nanjing, China). Primary antibodies against Cyclin-dependent kinase inhibitor 2B (P15) (cat. no. AB33457), Cyclin D1 (cat. no. ... although it collaborates with p53 to modify cyclin G2 appearance. Furthermore, this pathway regulates and cyclin G2 through ... Primers were labeled with 32P-ATP using T4 kinase. After the labeling reaction, the mixtures were cleared with G-50 minicolumns ... Cellular DNA was stained with propidium iodide (Nanjing KeyGen Biotech Co., Ltd.). Cell routine distributions were dependant on ...
CDKN2A and CDKN2B encode two specific inhibitors of cyclin-dependent kinase 4 (CDK4), i.e., p16INK4a and p15INK4b, respectively ...
CDKN2A and CDKN2B encode two specific inhibitors of cyclin-dependent kinase 4 (CDK4), i.e., p16INK4a and p15INK4b, respectively ...
This gene encodes a potent cyclin-dependent kinase inhibitor. The encoded protein binds to and inhibits the activity of cyclin- ... Cyclin-Dependent Kinase 5): CDK5 antibodies CDK5 ELISA Kits CDK5 Proteins CDK7 (Cyclin-Dependent Kinase 7): CDK7 antibodies ... Cyclin-Dependent Kinase 8): CDK8 antibodies CDK8 ELISA Kits CDK8 Proteins CDK9 (Cyclin-Dependent Kinase 9): CDK9 antibodies ... Cyclin-Dependent Kinase 3): CDK3 antibodies CDK3 ELISA Kits CDK3 Proteins CDKL3 (Cyclin-Dependent Kinase-Like 3): CDKL3 ...
The cell type-dependent different EBV latent gene expression patterns appear to be determined by the cellular epigenetic ... including several cyclin dependent kinase inhibitors (CDKIs) p14ARF, p15INK4a, and p16INK4a (reviewed in [13,57]). Importantly ... Cyclin dependent kinase inhibitor 2A; CtBP: C-terminal binding protein; HATs: Histone acetyltransferases; HDACs: Histone ... Cyclin dependent kinase inhibitor 2B; DNMT-1: DNA methyltransferase 1; HL: Hodgkins lymphoma; KDM6B: Lysine specific ...
  • These events resulted in upregulation of the Cdk4/6 inhibitor p15 (INK4B) and repression of the Cdk-activating phosphatase Cdc25A. (nih.gov)
  • 2002) studied the incidence of p15/INK4B gene deletions in 30 patients with T-cell acute lymphoblastic leukemia (T-ALL). (cags.org.ae)
  • This effect has been documented with the tumor suppressor genes p16 and p15 , whose products INK4a and INK4b are well known inhibitors of cyclin-dependent kinases. (jci.org)
  • The p21 family currently includes two related proteins, p27 Kip1 and p57 Kip2 , and the p16 family currently includes four related proteins: p16 INK4a (also variously known as MTS1, CDK4I and CDKN2), p15 INK4b (also known as MTS2), p18 INK4c , and p19 INK4d (reviewed in ref. 10 ). (pnas.org)
  • The INK4 proteins include p16 INK4a , p15 INK4b , p18 INK4c , and p19 INK4d , which are specific inhibitors of CDK4 and CDK6 ( 3 ). (asm.org)
  • TGF-β may inhibit cell cycle progression through regulation of cyclin-dependent kinase inhibitors p15 INK4B , p21 CIP1 , and p27 KIP1 ( 8 , 9 ) and induces apoptosis via activation of caspases ( 10 ). (pnas.org)
  • p15 INK4b / MTS 2 (Mitotic Inhibitor / Suppressor Protein) is a specific inhibitor of cdk 4 / cdk 6 and is periodically expressed during the cell cycle. (bioon.com.cn)
  • Reportedly, p15 INK4b expression is induced approximately 30 fold in human keratinocytes by treatment with TGF beta, suggesting that p15 INK4b may act as an effector of TGF beta mediated cell cycle arrest. (bioon.com.cn)
  • p15 INK4b is mapped to chromosome 9p21, a region of frequent loss in a wide variety of cancers. (bioon.com.cn)
  • p16 Ink4a , p15 Ink4b , p18 Ink4c and p19 Ink4d , and they bind specifically to Cdk4 and Cdk6, thereby negatively regulating their kinase activities and cell cycle progression. (diva-portal.org)
  • These 9p21.3 genes encode three cell cycle inhibitory proteins: p15 INK4b , p16 INK4a , and p14 ARF (Gil and Peters 2006 ). (springer.com)
  • In this study, we have systematically reviewed the studies of p15 INK4B promoter methylation in MM and quantified the association between p15 INK4B promoter methylation and MM using meta-analysis methods. (dovepress.com)
  • We observed that the frequency of p15 INK4B methylation is significantly higher in MM patients than in normal healthy controls. (dovepress.com)
  • This indicates that p15 INK4B inactivation through methylation plays an important role in the pathogenesis of MM. In addition, the frequency of p15 INK4B methylation was significantly higher in patients with MM than in those with asymptomatic monoclonal gammopathy of undetermined significance. (dovepress.com)
  • These results suggest that silencing of p15 INK4B gene expression by epigenetic modification such as promoter hypermethylation plays a role not only in the initiation of MM but also in plasma cell malignant transformation, disease progression, and development. (dovepress.com)
  • Spandidos, "Deregulation of the tumour suppressor genes p14ARF, p15 INK4b , p16INK4a and p53 in basal cell carcinoma," British Journal of Dermatology, vol. (thefreedictionary.com)
  • p15 INK4B gene methylation in acute lymphoblastic leukemia and its pronostic value. (thefreedictionary.com)
  • Methylation of the p15( INK4b ) gene in myelodysplastic syndromes is frequent and acquired during disease progression," Blood, vol. (thefreedictionary.com)
  • Moreover, depletion of ANRIL disrupts the binding of suppressor of zeste 12 protein homolog (Suz12), a component of PRC2, to INK4B locus, and increases the expression of p15 [49, 50]. (thefreedictionary.com)
  • Methylation of the p15( INK4B ) gene in myelodysplastic syndrome: It can be detected early at diagnosis or during disease progression and is highly associated with leukaemic transformation. (thefreedictionary.com)
  • p15( INK4B ) CpG island methylation in primary acute leukemia is heterogeneous and suggests density as a critical factor for transcriptional silencing. (thefreedictionary.com)
  • The p15( INK4b )/p16(INK4a)/RB1 pathway is frequently deregulated in human pituitary adenomas. (thefreedictionary.com)
  • CDK activity is regulated by 2 families of inhibitors: INK4 proteins, including INK4A (p16), INK4B (p15), INK4C (p18), and INK4D (p19), and the Cip and Kip family, which is composed of p21 (Cipl), p27 (Kipl), and p57 (Kip2) (5), (8). (thefreedictionary.com)
  • Immunohistochemical expression of P15 ( INK4B ) and SMAD4 in advanced gastric cancer. (thefreedictionary.com)
  • GDF-9 stimulated [ 3 H]thymidine incorporation, enhanced cell transition from G 0 /G 1 to S and G 2 /M phases (whereas both SB-431542 and PD-098059 attenuated these changes), increased mRNA and protein expression of cyclin D 1 and E, and decreased those of the cyclin-dependent kinase (CDK) inhibitors p15 INK4B and p16 INK4A . (scialert.net)
  • PD-098059 blocked Rb protein phorsphorylation and the increase in cyclin D 1 and E but not the decrease in p15 INK4B and p16 INK4A induced by GDF-9. (scialert.net)
  • GDF-9 stimulates hLG cell proliferation by stimulating cyclin D 1 and E and suppressing p15 INK4B and p16 INK4A via both Smad-dependent and Smad-independent pathways. (scialert.net)
  • The promoter region of the cyclin-dependent kinase inhibitor p15(INK4B) contains a CpG island that is hypermethylated in many hematologic malignancies. (elsevier.com)
  • Cameron, EE , Baylin, SB & Herman, JG 1999, ' p15(INK4B) CpG island methylation in primary acute leukemia is heterogeneous and suggests density as a critical factor for transcriptional silencing ', Blood , vol. 94, no. 7, pp. 2445-2451. (elsevier.com)
  • Down-regulation of P15 INK4B and up-regulation of Bcl-2 by ANRIL may partially explain ANRIL-induced EOC cell proliferation. (oncotarget.com)
  • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) is a Protein Coding gene. (genecards.org)
  • The p15 tumor suppressor (CDKN2B) is located in the same region as p16 ( CDKN2A ), and is also involved in cell cycle, senescence and cancer. (senescence.info)
  • Objectives Because post-transcriptional mechanisms modulate levels of p16 (encoded by CDKN2A ) and p15 (encoded by CDKN2B ), we tested whether interferon-γ regulates the expression of these proteins and the effect of the 9p21 genotype. (onlinejacc.org)
  • The common genetic variant located in the vicinity of the genes encoding the cyclin-dependent kinase inhibitors p15 ( CDKN2B ) and p16/ARF ( CDKN2A ) on the short arm of chromosome 9 at 9p21.3 contributes to the risk of CAD by an unknown mechanism that is independent of known risk factors ( 1-3 ). (onlinejacc.org)
  • Cyclin-dependent kinase inhibitor 2B ( CDKN2B , also known as p15 ) is a gene that encodes a protein that binds to CDK4 or CDK6 and inhibits their activation. (mycancergenome.org)
  • [email protected]#The aim of this study is to establish whether cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) gene polymorphisms are associated with premature triple-vessel disease (PTVD). (bvsalud.org)
  • The p16, p15 and p14 genes are widely known as tumor suppressor genes in human medicine. (ceek.jp)
  • 2000) examined 168 tumor tissue, 20 schistosomal tissue, and 50 normal tissue samples for the status of the p15 genes using the polymerase chain reaction and by sequencing the DNA fragments produced during PCR. (cags.org.ae)
  • The results showed 23.3% of the patients to have deletions of the p15 gene indicating that loss of tumor suppression involves inactivation of either or both p15 and p16 genes on 9p21 in T-ALL. (cags.org.ae)
  • The deletion of p16 and p15 genes was associated with poor differentiation grade and presence of bilharziasis. (cags.org.ae)
  • 1 5-7 Several TSGs altered by hypermethylation encode genes involved in cell cycle regulation (eg, Rb, p16 , p15 , VHL). (bloodjournal.org)
  • Rb inactivation leads to expression of E2F-dependent genes such as thymidine kinase, DNA polymerase-α, cdc2, and cyclin A ( 5 ), which are not expressed in senescent cells ( 6 ), indicating that the failure to phosphorylate Rb is important in the growth arrest of senescent cells. (pnas.org)
  • The improved cardiac phenotype was associated with attenuation of heart and cardiomyocyte size, less cardiac fibrosis, lower expression of atrial and B-type natriuretic peptide genes, attenuation of profibrotic markers and increased expression of p15 (a miR-154 target and cell cycle inhibitor). (nature.com)
  • Thus, targeting genes such as microRNAs (miRNAs), that are regulated by the cardioprotective kinase PI3K(p110α), may represent a promising therapeutic approach to improve function of the failing heart. (nature.com)
  • The analysis of epigenetic changes on RASSF1A, p16 , and p15 tumor suppressor genes in serum DNA may be a valuable biomarkers for early detection in populations at high risk of HCC. (aacrjournals.org)
  • Importantly, cyclin K and cyclin D1b have no major action on cell cycle or apoptosis regulatory genes. (biomedcentral.com)
  • Hoxa-10 mutants express a stromal cell proliferation defect that is accompanied by quantitative or spatial alterations in the expression of two cyclin-dependent kinase inhibitor genes, p57 and p15. (broadinstitute.org)
  • Specifically, it prevents Myc binding to promoter E-boxes and transactivation of target genes while retaining Miz-1 dependent binding to promoters and transrepression. (pubmedcentralcanada.ca)
  • Co-treatment with chaetocin and HDAC inhibitor trichostatin A (TSA) dramatically increased apoptosis and produced greater activation of genes. (bvsalud.org)
  • The p16 family (p15, p16, p18 and p19) binds to and inhibits the activities of CDK4 and CDK6. (biomedcentral.com)
  • p15 interacts strongly with cyclin-dependent kinases CDK4 and CDK6, and inhibits their ability to interact with cyclins D, thereby blocking the CyclinD/CDK complex from phosphorylating the retinobloastoma protein (RB1). (cags.org.ae)
  • This gene encodes a cyclin-dependent kinase inhibitor, which forms a complex with CDK4 or CDK6, and prevents the activation of the CDK kinases, thus the encoded protein functions as a cell growth regulator that controls cell cycle G1 progression. (genecards.org)
  • The members of this family (p16INK4a, p15INK4b, p18INK4c, p19INK4d) are inhibitors of CDK4 (hence their name INhibitors of CDK4), and of CDK6. (wikipedia.org)
  • When they bind to CDK4 and CDK6, they induce an allosteric change that leads to the formation of CDK-INK4 complexes rather than CDK-cyclin complexes. (wikipedia.org)
  • 23 24 p16 INK4a exerts a tumor-suppressive function by specifically interfering with the catalytic activity of complexes between cyclin D and cyclin-dependent kinase 4 (CDK4) or CDK6. (nature.com)
  • Ribociclib are US FDA approved CDK4 and CDK6 inhibitors for the treatment of estrogen receptor positive/ HER2 negative advanced breast cancer. (wikipedia.org)
  • p15INK4b is a specific inhibitor of cdk4/cdk6 and is periodically expressed during cell cycle. (genetex.com)
  • Furthermore, the senescent-cell-cycle arrest occurs prior to the accumulation of the Cdk4-Cdk6 inhibitor p16 Ink4a , suggesting that p21 may be sufficient for this event. (asm.org)
  • Instead, the cyclin D1-Cdk4 and cyclin D1-Cdk6 complexes in these cells are associated with an increased amount of p21, suggesting that p21 may be responsible for inactivation of both cyclin E- and cyclin D1-associated kinase activity at the early stage of senescence. (asm.org)
  • Phosphorylation of pRb during G 1 phase is carried out by cyclin D-Cdk4 and cyclin D-Cdk6 (cyclin D-Cdk4/6) and cyclin E-Cdk2 complexes ( 44 , 50 , 55 ). (asm.org)
  • The BCH inhibited the expression of cyclin-dependent protein kinase 6 (CDK6) in a time-dependent manner. (biomedsearch.com)
  • These results suggest that, in KB cells, the inhibition of LAT1 by BCH causes cell cycle arrest at G1 phase by inhibiting cyclin D3-CDK6 complex whereas increasing expression of a CDK inhibitor p27. (biomedsearch.com)
  • To determine a possible mechanism by which senescent human fibroblasts maintain a hypophosphorylated Rb, we examined the expression levels and interaction of the Rb kinases, CDK4 and CDK6, and the cyclin-dependent kinase inhibitors p21 and p16 in senescent HDFs. (pnas.org)
  • Immunodepletion analysis of p21 and p16 from the senescent cell extracts revealed that p16 is the major CDK inhibitor for both CDK4 and CDK6 kinases. (pnas.org)
  • Immunoprecipitation of CDK4 and CDK6 and their associated proteins from radiolabeled extracts from senescent HDFs showed no other CDK inhibitors. (pnas.org)
  • Three cyclin-dependent kinases, CDK2, CDK4, and CDK6, are involved in the phosphorylation of the Rb protein (reviewed in ref. 5 ). (pnas.org)
  • Antigen receptor signaling or exposure to growth factors triggers de novo synthesis of D-type cyclins, which then associate with their catalytic partners CDK4 or CDK6. (asm.org)
  • A gene on chromosome 9p21 that encodes a member of the INK4 family of cyclin-dependent kinase inhibitors, which form a complex with CDK4 or CDK6, preventing activation of CDK kinases and thus acting as cell growth regulators by controlling cell cycle progression through G1. (thefreedictionary.com)
  • Cyclin-dependent kinase inhibitors (CDKIs) are proteins that bind to and inhibit the activity of CDKs. (biomedcentral.com)
  • Enforced expression of INK4 proteins can lead to G1 arrest by promoting redistribution of Cip/Kip proteins and blocking cyclin E-CDK2 activity. (wikipedia.org)
  • INK4 proteins are cell-cycle inhibitors. (wikipedia.org)
  • Seven cyclin-dependent kinase inhibitor proteins have thus far been identified. (wikipedia.org)
  • Mutations in this gene as well as in its related proteins including D-type cyclins, p16(INK4a) and Rb were all found to be associated with tumorigenesis of a variety of cancers. (wikipedia.org)
  • Although Smad proteins are considered important mediators ( 12 , 23 , 24 ), Smad-independent TGF-β signaling has been demonstrated, involving predominantly MAP kinase pathways. (pnas.org)
  • These proteins form active Cdk:cyclin complexes that phosphorylate specific substrates. (diva-portal.org)
  • Cyclin D proteins bind to enzymes called CDK4/6 and together they form heterodimers. (springer.com)
  • The expression of both proteins decreases after birth and in the cochlea of E18.5 embryonic Igf1(-/-) null mice, the balance of the main IGF related signalling pathways is altered, with lower activation of Akt and ERK1/2 and stronger activation of p38 kinase. (whiterose.ac.uk)
  • CCND1 gene is alternatively spliced to produce two cyclin D1 mRNA isoforms which are translated in two proteins: cyclin D1a and cyclin D1b. (biomedcentral.com)
  • The two corresponding proteins cyclin D1a and D1b differ only in the last 55 amino acids of the carboxy-terminus. (biomedcentral.com)
  • The antiproliferative effects of K + channel blockers and veratridine were still present in OP cells isolated from INK4a −/− mice, lacking the cyclin-dependent kinase inhibitors p16 INK4a and p19 ARF . (jneurosci.org)
  • The activity of this kinase is restricted to the G1-S phase, which is controlled by the regulatory subunits D-type cyclins and CDK inhibitor p16 INK4a . (wikipedia.org)
  • The tumor suppressor gene p16 (also called MTS1, CDKN2 and INK4A) is a cyclin-dependent kinase (CDK) inhibitor and a negative cell cycle regulator ( 1 ). (jcancer.org)
  • Cyclins regulate the cell cycle in association with cyclin dependent kinases (CDKs). (biomedcentral.com)
  • CDKs are under inhibitory control of cyclin dependent kinase inhibitors (CDKIs). (biomedcentral.com)
  • The progression of cells through the cell cycle is regulated by a family of protein kinases known as the cyclin-dependent kinases (CDKs). (biomedcentral.com)
  • Cyclins function as the positive regulators of CDKs. (biomedcentral.com)
  • Cyclins and CDKs assemble into complexes with one another as cells progress through G1 phase, cyclins being required to activate the serine-threonine kinase activity of their catalytic partners. (biomedcentral.com)
  • Another potent CDK inhibitor, p21 WAF1/CIP1 , is a downstream effector of p53 and controls cell cycle progression by inhibiting the activity of a broader range of CDKs. (nature.com)
  • See also CDK inhibitor for inhibitors of various CDKs. (wikipedia.org)
  • The activating cyclins for these CDKs, cyclins D1 and E, are present in senescent cells at similar or elevated levels relative to early passage cells ( 8 ). (pnas.org)
  • In mammalian cells, cell cycle traversal is regulated by cyclins and cyclin-dependent kinases (CDKs) that are in turn controlled by CDK inhibitors (CKIs) ( 31 ). (asm.org)
  • Progression through the G1, S, G2 and M phases of the cell cycle is controlled by cyclin-dependent kinases (Cdks) and cyclins. (diva-portal.org)
  • Cyclin-dependent kinases (CDKs) have been considered promising drug targets for a number of years, but most CDK inhibitors have failed rigorous clinical testing. (aspetjournals.org)
  • Cancer is a disease of uncontrolled proliferation, and since CDKs are a central component of the cell cycle engine, great effort has been expended in developing CDK inhibitors as anticancer agents. (aspetjournals.org)
  • The gene codes for a protein, p15, which is an inhibitor of cyclin dependent kinases, and thus, acts as a negative regulator of cell proliferation. (cags.org.ae)
  • Mutations in the gene cause the protein to lose their capacity to block the Cyclin D/CDK activation, resulting in uncontrolled cell proliferations, and development of malignancies. (cags.org.ae)
  • Deletion of the p15 gene was observed in 36 bladder tumors. (cags.org.ae)
  • Clinical examination of the patients was followed by laboratory investigation, involving complete hemogram, bone marrow aspiration and examination, flow cytometric studies for B and T cell precursor markers, and PCR using primers specific for the p15 gene. (cags.org.ae)
  • Follow-up of the patients showed a complete remission (CR) rate of 63.6% in patients with no deletions, in comparison to 100% CR in patients with deletions of p15 gene. (cags.org.ae)
  • 2004) evaluated p15 gene deletion in bladder carcinoma among Egyptian patients, in relation to different clinicopathological features of the tumors and presence or absence of bilharziasis. (cags.org.ae)
  • P15 gene deletions were examined by polymerase chain reaction (PCR). (cags.org.ae)
  • In all normal samples, p15 gene was detected. (cags.org.ae)
  • P15 gene was deleted in 30.2% (32/106) of bladder tumors. (cags.org.ae)
  • GO annotations related to this gene include protein kinase binding and cyclin-dependent protein serine/threonine kinase inhibitor activity . (genecards.org)
  • Cyclin-dependent kinase 4 also known as cell division protein kinase 4 is an enzyme that in humans is encoded by the CDK4 gene . (wikipedia.org)
  • The protein encoded by this gene is a member of the Ser/Thr protein kinase family . (wikipedia.org)
  • This kinase was shown to be responsible for the phosphorylation of retinoblastoma gene product ( Rb ). (wikipedia.org)
  • Hypermethylation in the 5′ p15 gene region was detected in 15 of 23 patients (65%), whereas the 5′ p16 region was unmethylated in all patients. (bloodjournal.org)
  • This protein kinase is highly similar to the gene products of S. cerevisiae cdc28, and S. pombe cdc2. (antibodies-online.com)
  • The protein encoded by this gene is a member of the cyclin-dependent protein kinase (CDK) family. (antibodies-online.com)
  • The cell type-dependent different EBV latent gene expression patterns appear to be determined by the cellular epigenetic machinery and similarly viral oncoproteins recruit epigenetic regulators in order to deregulate the cellular gene expression profile resulting in several human cancers. (mdpi.com)
  • The gene expression profiling approach delineates complex context-dependent signaling pathways and transcriptional events that determine epithelial cell plasticity controlled by TGF-β. (pnas.org)
  • Although both phosphatidylinositol-3 kinase and extracellular response kinase (ERK) mitogen-activated protein (MAP) kinase signaling pathways have been implicated in TGF-β-induced EMT ( 20 , 21 ), their specific roles and proximal target gene programs in EMT remain unclear. (pnas.org)
  • Hypermethylation of p16 , a cyclin-dependent kinase inhibitor gene that regulates the cell cycle, has been detected frequently in human cancers ( 10 ). (aacrjournals.org)
  • p15 , another cyclin-dependent kinase inhibitor gene adjacent to p16 on chromosome 9p21, has been postulated to be a tumor suppressor modulating pRb phosphorylation. (aacrjournals.org)
  • The p15 gene which encodes a cyclin-dependent kinase inhibitor, is located in the 9p21 chromosomal region that is frequently deleted in human bladder transitional cell carcinomas (TCCs). (ebscohost.com)
  • Amplification of the cyclin D1 gene is preferentially found in esophageal cancer, whereas amplification of c- met is common in gastric cancer. (springer.com)
  • The cyclin E gene amplification is frequently associated with both gastric and colorectal cancers. (springer.com)
  • Deletion of the cyclin-dependent kinase inhibitor gene is often found in esophageal carcinoma cell lines. (springer.com)
  • A cyclin-dependent kinase inhibitor protein is a protein which inhibits the enzyme cyclin-dependent kinase (CDK). (wikipedia.org)
  • Hsp27 also inhibits apoptosis in stressed cells, regulating upstream signaling pathways such as Akt activation by forming a signaling complex with p38 mitogen-activated protein kinase (MAPK) and MAPKAP-2, a kinase that phosphorylates Akt ( 11 - 14 ). (aacrjournals.org)
  • Here we report a transcriptome screen of genetic programs of TGF-β-induced EMT in human keratinocytes and propose functional roles for extracellular response kinase (ERK) mitogen-activated protein kinase signaling in cell motility and disruption of adherens junctions. (pnas.org)
  • INK4 is a family of cyclin-dependent kinase inhibitors (CKIs). (wikipedia.org)
  • The irreversible G 1 arrest in senescent human diploid fibroblasts is probably caused by inactivation of the G 1 cyclin-cyclin-dependent kinase (Cdk) complexes responsible for phosphorylation of the retinoblastoma protein (pRb). (asm.org)
  • Cell cycle progression is delayed or stopped by cyclin-dependent kinase inhibitors, abbreviated CDIs, CKIs or CDKIs. (wikipedia.org)
  • CKIs act as brakes for the cell cycle, restraining the activity of cyclin-CDK complexes to maintain cells in the quiescent G 0 /G 1 phase or to induce cell cycle exit in proliferating cells. (asm.org)
  • This process is in part regulated by a family of Cdk inhibitors (CKIs) called the Ink4 family (Inhibitors of Cdk4). (diva-portal.org)
  • There are two classes of CKI: the INK4 inhibitors and the Cip/Kip inhibitors ( 31 , 41 ). (asm.org)
  • Blockage of K + channels and membrane depolarization also caused accumulation of the cyclin-dependent kinase inhibitors p27 Kip1 and p21 CIP1 in OP cells. (jneurosci.org)
  • Here, we have identified the cyclin-dependent kinase inhibitor p27 Kip1 as a critical regulator of the CD8 T-cell homeostasis at all phases of the T-cell response to an acute viral infection in mice. (asm.org)
  • mRNA and protein expression patterns in these mice and in cyclin D1-null mice suggest that Chx10 influences p27 Kip1 at a post-transcriptional level, through a mechanism that is largely dependent on cyclin D1. (biologists.org)
  • By contrast, there was an increase in the nuclear accumulation of FoxM1 and a corresponding decrease in the nuclear cyclin-dependent kinase inhibitor p27(Kip1). (whiterose.ac.uk)
  • Pfn1 overexpression results in increased protein stability of p27 kip1 (p27 - a major cyclin-dependent kinase inhibitor) and marked elevation in the overall cellular level of p27. (pubmedcentralcanada.ca)
  • We show that the Cdk inhibitor p21 Sdi1,Cip1,Waf1 , which accumulates progressively in aging cells, binds to and inactivates all cyclin E-Cdk2 complexes in senescent cells, whereas in young cells only p21-free Cdk2 complexes are active. (asm.org)
  • The finding that senescent HDF contain elevated amounts of the ubiquitously acting cyclin-dependent kinase inhibitor (CKI) p21 Sdi1,Cip1,Waf1 (p21) ( 40 ) suggested instead that cyclin E-Cdk2 complexes in senescent cells might be inactivated by increased binding of p21. (asm.org)
  • It has been hypothesized that voltage-dependent K + channel activity could regulate mitogenesis in the nervous system by maintaining the membrane potential hyperpolarized, a condition necessary for progression through G1 phase restriction points ( Wonderlin and Strobl, 1996 ). (jneurosci.org)
  • and (2) cyclins and cyclin-dependent kinase inhibitors (cdkis) known to regulate cell cycle progression through this phase are affected by ion channel activity or changes in membrane potential. (jneurosci.org)
  • It is a catalytic subunit of the protein kinase complex that is important for cell cycle G1 phase progression. (wikipedia.org)
  • p15 , a target of transforming growth factor-β signaling, 16 is an inhibitor of the cyclin-dependent kinase-4 17 18 and a negative regulator of the G 1 /S progression within the cell cycle. (bloodjournal.org)
  • Progression from one phase to another is controlled by cyclin dependent kinases (CDK) and their activators, cyclins. (antibodies-online.com)
  • The Cdk:cyclin complexes of the G1/S transition regulate the progression of cells into the S phase by phosphorylating the retinoblastoma protein (Rb). (diva-portal.org)
  • Cyclin D1 is a key actor for the development and progression of various cancers including hematological malignancies. (biomedcentral.com)
  • 25 This inhibitory effect on cyclin D/CDK4(6) complexes prevents phosphorylation of the retinoblastoma protein (Rb) and the subsequent release of transcription factors that are required for passage into and through S phase, in particular members of the E2F transcription factor family. (nature.com)
  • Accordingly, cyclin D1-associated phosphorylation of pRb at Ser-780 is lacking even in newly senescent fibroblasts that have a low amount of p16. (asm.org)
  • EGF increases the phosphorylation of cAMP-responsive element-binding protein (p-CREB) and its association with the coregulator, CCAAT/enhancer binding protein β, whereas blocking the EGF-induced ERK1/2 phosphorylation with MAPK inhibitors (PD98059/U0126) markedly reduced these effects. (scialert.net)
  • The PEST sequence which controls protein turn-over and the threonine 286 (Thr286), the site of phosphorylation by glycogen synthase kinase-3β which promotes the nuclear export of cyclin D1 and its degradation through the proteasome pathway [ 2 , 3 ], are present only in cyclin D1a. (biomedcentral.com)
  • This protein is a catalytic subunit of the highly conserved protein kinase complex known as M-phase promoting factor (MPF), which is essential for G1/S and G2/M phase transitions of eukaryotic cell cycle. (antibodies-online.com)
  • It is a catalytic subunit of the cyclin-dependent protein kinase complex, whose activity is restricted to the G1-S phase, and essential for cell cycle G1/S phase transition. (antibodies-online.com)
  • The purpose of this study was to examine the effect of 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH), an inhibitor of L-type amino acid transporters, on the cell growth suppression in KB human oral cancer cells and to study the roles of cell cycle regulatory factors in the BCH-induced growth inhibition. (biomedsearch.com)
  • Canonical BMP9 signaling via activin-like kinase-1-Smad1/5/9 was disrupted by inhibition of Notch signaling, even in the absence of exogenous DLL4. (ahajournals.org)
  • Cyclin E forms complexes during this interval with CDK2. (biomedcentral.com)
  • In contrast, we have shown previously that although serum-stimulated senescent HDF (IMR90) have abundant cyclin E-Cdk2 complexes, they lack cyclin E-associated kinase activity, a finding consistent with their failure to phosphorylate pRb ( 14 ). (asm.org)
  • Regulation of Cdk2 activity by activating (Thr-160) and inhibiting phosphorylations (Thr-14, Tyr-15) did not account for the lack of cyclin E-Cdk2 kinase activity in senescent cells, i.e., even though approximately one-half of the cyclin E-associated Cdk2 was phosphorylated on Thr-160, treatment with Cdc25 phosphatase to dephosphorylate Thr-14 and Tyr-15 did not increase activity. (asm.org)
  • These cyclin-CDK complexes, as well as cyclin E-CDK2 complexes later in the cell cycle, phosphorylate retinoblastoma protein (Rb). (asm.org)
  • These creative ways to develop CDK inhibitors are presented along with crystal structures of these agents complexed with CDK2 to highlight differences in their binding sites and mechanisms of action. (aspetjournals.org)
  • Inhibitors of mammalian G1 cyclin-dependent kinases. (abnova.com)
  • In mammalian cells, two distinct families of CDK inhibitors have been characterized, represented by two prototype CDK inhibitors, p21 and p16. (pnas.org)
  • In this study we tested the expression of CDKIs p15, p16, p21 and p27 by immunohistochemistry to determine the role of CDKIs in the initiation of primordial follicle growth. (biomedcentral.com)
  • p15, p16, p21 and p27 in mouse ovaries by immunohistochemistry to assess whether the initiation of primordial follicle growth was associated with the expression of CDKIs. (biomedcentral.com)
  • [5] Ser/Thr-kinase component of cyclin D-CDK4 (DC) complexes that phosphorylate and inhibit members of the retinoblastoma (RB) protein family including RB1 and regulate the cell-cycle during G1/S transition. (wikipedia.org)
  • The expression of p15 protein was undetectable in 38 bladder tumors by Western blot analysis. (cags.org.ae)
  • Unlike in solid tumors, the 5′ region of p15 but not p16 is frequently methylated in AML 5 7 and MDS. (bloodjournal.org)
  • Here we show that deletion of the Miz1 POZ domain, which is critical for Miz1 function, restrains the development of skin tumors in a model of chemically-induced, Ras-dependent tumorigenesis. (jove.com)
  • To test the tumorigenic potential of cyclin D1b in vivo , we generated cell clones derived from the non- CCND1 expressing MM LP-1 cell line, synthesizing either cyclin D1b or cyclin K, a structural homolog and viral oncogenic form of cyclin D1a. (biomedcentral.com)
  • Two major classes of CDK inhibitors have been identified. (biomedcentral.com)
  • The purpose of this review is to provide a broad overview of the development of various classes of CDK inhibitors. (aspetjournals.org)
  • Both GnRH I and II activated protein kinase C, ERK1/2, and c-Jun N-terminal kinase to mediate their effects on trophoblast invasion, whereas only GnRH II elicited invasion-promoting action through transactivating the tyrosine kinase activity of epidermal growth factor receptor in trophoblasts. (scialert.net)
  • Also phosphorylates SMAD3 in a cell-cycle-dependent manner and represses its transcriptional activity. (wikipedia.org)
  • Using these primers, the expression of p16, p15 and p14 mRNAs could be individually evaluated by reverse transcriptase polymerase chain reaction. (ceek.jp)
  • Results In all cells tested-except HUVECs where expression was not modulated by interferon-γ-regardless of 9p21.3 genotype, interferon-γ increased the expression of p16 and p15. (onlinejacc.org)
  • Both isoforms possess the N-terminal domain, necessary for retinoblastoma protein (pRb) binding, the cyclin box, required for cyclin-dependent kinase (CDK) binding and activation and the central region, implicated in transcriptional regulation. (biomedcentral.com)
  • Among 12 patients with hypermethylation sequentially analyzed after at least one course of decitabine treatment, a decrease in p15 methylation occurred in 9 and was associated with clinical response. (bloodjournal.org)
  • Immunohistochemical staining for p15 protein in bone marrow biopsies from 8 patients with p15 hypermethylation revealed low or absent expression in 4 patients, which was induced to normal levels during decitabine treatment. (bloodjournal.org)
  • In conclusion, frequent, selective p15 hypermethylation was reversed in responding MDS patients following treatment with a methylation inhibitor. (bloodjournal.org)
  • RASSF1A had the highest frequency of hypermethylation with 35 (70%) cases having at least one positive sample compared with 22 (44%) for p16 and 12 (22%) for p15 . (aacrjournals.org)
  • Our results suggest that the transcriptional silencing of p15 in conjunction with aberrant hypermethylation is best understood as an evolutionary process that involves progressively increasing methylation of the entire p15 CpG island. (elsevier.com)
  • Moreover, even in the late stage of senescence when p16 is high, cyclin D1-Cdk4 complexes are persistent, albeit reduced by ≤50% compared to young cells. (asm.org)
  • A role of the CDK inhibitors in senescence was revealed by the isolation of a cDNA of a highly expressed message in senescent cells that encoded the CDK inhibitor, p21 ( 9 ). (pnas.org)
  • HDAC inhibitor pathway activation results in apoptosis and decreased tumor burden following a 7-day quisinostat treatment in the Pten fl/fl ;hSS2 mouse model of synovial sarcoma. (aacrjournals.org)
  • Moreover, we showed that EZH2 depletion sensitized pancreatic cancer cells to doxorubicin and gemcitabine, which leads to a significant induction of apoptosis, suggesting that the combination of EZH2 inhibitors and standard chemotherapy could be a superior potential treatment for pancreatic cancer. (aacrjournals.org)
  • Histone deacetylase (HDAC) inhibitors inhibit deacetylases and accumulate high levels of acetylation lead to cell cycle arrest and apoptosis. (bvsalud.org)
  • NS5B is the RNA-dependent RNA polymerase [ 7 ] and NS2 and NS3 represent viral proteases. (hindawi.com)
  • The p21 family (p21, p27, p28 and p57) can bind to broad range of CDK-cyclin complexes and inhibit their activities. (biomedcentral.com)
  • Two critical pathways are delta-like 4 (DLL4)/Notch and BMP9/activin-like kinase-1 (ALK1), which can display cooperative signal transduction 1 , 2 and inhibit hypersprouting to maintain appropriate capillary density. (ahajournals.org)
  • The programmed cell death-1 (PD)-1 receptor (CD279) is a potent T cell inhibitor with a critical role in peripheral tolerance, but it can also compromise anti-viral and antitumor T cell responses. (nih.gov)
  • Potent inhibitor. (genecards.org)
  • 5-Azacytidine and 5-Aza-2′-deoxycytidine (decitabine), 2 potent inhibitors of cytosine methylation, 8 have shown strong antileukemic activity 9 in acute myeloid leukemia (AML). (bloodjournal.org)
  • We examined p15 and p16 methylation status in bone marrow mononuclear cells from patients with high-risk MDS during treatment with decitabine, using a methylation-sensitive primer extension assay (Ms-SNuPE) to quantitate methylation, and denaturing gradient gel electrophoresis (DGGE) and bisulfite-DNA sequencing to distinguish individually methylated alleles. (bloodjournal.org)
  • Methylation-specific PCR was used to determine the methylation status of p16, p15 , and ras association domain family 1A ( RASSF1A ). (aacrjournals.org)
  • Component of the ternary complex, cyclin D/CDK4/CDKN1B, required for nuclear translocation and activity of the cyclin D-CDK4 complex. (wikipedia.org)
  • Two of the six canine lymphoid tumor cell lines did not express detectable levels of p16, p15 and p14 mRNAs, and wide-ranging deletions in the p15-p14-p16 genomic locus were suspected. (ceek.jp)
  • Deletion of the p15-p14-p16 genomic locus could be one of the molecular aberrations in canine lymphoid tumor cells. (ceek.jp)
  • Membrane potential-dependent transport of essential metabolic substrates during the cell cycle and/or volume regulation could also play a role (for review, see Wonderlin and Strobl, 1996 ). (jneurosci.org)
  • This work raises critical questions about the nature and regulation of the demethylases that erase p15 methylation in these cells. (jci.org)
  • Genome-wide analysis of LP-1-derived cells indicated that several cellular processes were altered by cyclin D1b and/or cyclin K expression such as cell metabolism, signal transduction, regulation of transcription and translation. (biomedcentral.com)
  • Ataxia-telangiectasia-mutated (ATM)-dependent DNA-damage response, non-homologous end joining, and homologous recombination pathways coordinately contribute to repairing DSBs in higher eukaryotes. (frontiersin.org)
  • Recently, the capabilities of these cytokines to support DNA repair pathways and the ATM-dependent DNA response have been demonstrated. (frontiersin.org)
  • Both NAD-dependent and Pttg1-dependent pathways were responsible for mediating different subsets of these alterations, also incorporating changes in VCP/p97 localization and Ube1 expression. (biomedcentral.com)
  • Objective- Bone morphogenetic protein-9 (BMP9)/activin-like kinase-1 and delta-like 4 (DLL4)/Notch promote endothelial quiescence, and we aim to understand mechanistic interactions between the 2 pathways. (ahajournals.org)
  • Similarly, DLL4 activity was suppressed when the basal activin-like kinase-1-Smad1/5/9 pathway was inhibited, showing that these pathways are interdependent. (ahajournals.org)
  • Conclusions- DLL4/Notch and BMP9/activin-like kinase-1 signaling rely on each other's pathways for full activity. (ahajournals.org)