Cyclin dependent kinase inhibitor p18. Medical search

A cyclin-dependent kinase inhibitor that coordinates the activation of CYCLIN and CYCLIN-DEPENDENT KINASES during the CELL CYCLE. It interacts with active CYCLIN D complexed to CYCLIN-DEPENDENT KINASE 4 in proliferating cells, while in arrested cells it binds and inhibits CYCLIN E complexed to CYCLIN-DEPENDENT KINASE 2.

A cyclin-dependent kinase inhibitor that mediates TUMOR SUPPRESSOR PROTEIN P53-dependent CELL CYCLE arrest. p21 interacts with a range of CYCLIN-DEPENDENT KINASES and associates with PROLIFERATING CELL NUCLEAR ANTIGEN and CASPASE 3.

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

A large family of regulatory proteins that function as accessory subunits to a variety of CYCLIN-DEPENDENT KINASES. They generally function as ENZYME ACTIVATORS that drive the CELL CYCLE through transitions between phases. A subset of cyclins may also function as transcriptional regulators.

Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.

A product of the p16 tumor suppressor gene (GENES, P16). It is also called INK4 or INK4A because it is the prototype member of the INK4 CYCLIN-DEPENDENT KINASE INHIBITORS. This protein is produced from the alpha mRNA transcript of the p16 gene. The other gene product, produced from the alternatively spliced beta transcript, is TUMOR SUPPRESSOR PROTEIN P14ARF. Both p16 gene products have tumor suppressor functions.

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

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

High molecular weight proteins found in the MICROTUBULES of the cytoskeletal system. Under certain conditions they are required for TUBULIN assembly into the microtubules and stabilize the assembled microtubules.

A key regulator of CELL CYCLE progression. It partners with CYCLIN E to regulate entry into S PHASE and also interacts with CYCLIN A to phosphorylate RETINOBLASTOMA PROTEIN. Its activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P27 and CYCLIN-DEPENDENT KINASE INHIBITOR P21.

Protein encoded by the bcl-1 gene which plays a critical role in regulating the cell cycle. Overexpression of cyclin D1 is the result of bcl-1 rearrangement, a t(11;14) translocation, and is implicated in various neoplasms.

A cyclin subtype that has specificity for CDC2 PROTEIN KINASE and CYCLIN-DEPENDENT KINASE 2. It plays a role in progression of the CELL CYCLE through G1/S and G2/M phase transitions.

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

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

Cyclin-dependent kinase 4 is a key regulator of G1 PHASE of the CELL CYCLE. It partners with CYCLIN D to phosphorylate RETINOBLASTOMA PROTEIN. CDK4 activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P16.

A family of cell cycle-dependent kinases that are related in structure to CDC28 PROTEIN KINASE; S CEREVISIAE; and the CDC2 PROTEIN KINASE found in mammalian species.

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

A potent inhibitor of CYCLIN-DEPENDENT KINASES in G1 PHASE and S PHASE. In humans, aberrant expression of p57 is associated with various NEOPLASMS as well as with BECKWITH-WIEDEMANN SYNDROME.

A cell line derived from cultured tumor cells.

Agents that inhibit PROTEIN KINASES.

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

The period of the CELL CYCLE preceding DNA REPLICATION in S PHASE. Subphases of G1 include "competence" (to respond to growth factors), G1a (entry into G1), G1b (progression), and G1c (assembly). Progression through the G1 subphases is effected by limiting growth factors, nutrients, or inhibitors.

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

A cyclin subtype that is transported into the CELL NUCLEUS at the end of the G2 PHASE. It stimulates the G2/M phase transition by activating CDC2 PROTEIN KINASE.

A cyclin subtype that is specific for CYCLIN-DEPENDENT KINASE 4 and CYCLIN-DEPENDENT KINASE 6. Unlike most cyclins, cyclin D expression is not cyclical, but rather it is expressed in response to proliferative signals. Cyclin D may therefore play a role in cellular responses to mitogenic signals.

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

A group of cell cycle proteins that negatively regulate the activity of CYCLIN/CYCLIN-DEPENDENT KINASE complexes. They inhibit CELL CYCLE progression and help control CELL PROLIFERATION following GENOTOXIC STRESS as well as during CELL DIFFERENTIATION.

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

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

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

Product of the retinoblastoma tumor suppressor gene. It is a nuclear phosphoprotein hypothesized to normally act as an inhibitor of cell proliferation. Rb protein is absent in retinoblastoma cell lines. It also has been shown to form complexes with the adenovirus E1A protein, the SV40 T antigen, and the human papilloma virus E7 protein.

Cyclin-dependent kinase 6 associates with CYCLIN D and phosphorylates RETINOBLASTOMA PROTEIN during G1 PHASE of the CELL CYCLE. It helps regulate the transition to S PHASE and its kinase activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P18.

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

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

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

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

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

Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.

Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.

Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.

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

A cyclin D subtype which is regulated by GATA4 TRANSCRIPTION FACTOR. Experiments using KNOCKOUT MICE suggest a role for cyclin D2 in granulosa cell proliferation and gonadal development.

Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.

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

Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.

An E2F transcription factor that interacts directly with RETINOBLASTOMA PROTEIN and CYCLIN A and activates GENETIC TRANSCRIPTION required for CELL CYCLE entry and DNA synthesis. E2F1 is involved in DNA REPAIR and APOPTOSIS.

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

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

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

The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.

Established cell cultures that have the potential to propagate indefinitely.

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

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

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

A transcription factor that possesses DNA-binding and E2F-binding domains but lacks a transcriptional activation domain. It is a binding partner for E2F TRANSCRIPTION FACTORS and enhances the DNA binding and transactivation function of the DP-E2F complex.

Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.

Nuclear antigen with a role in DNA synthesis, DNA repair, and cell cycle progression. PCNA is required for the coordinated synthesis of both leading and lagging strands at the replication fork during DNA replication. PCNA expression correlates with the proliferation activity of several malignant and non-malignant cell types.

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

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

A cyclin G subtype that is constitutively expressed throughout the cell cycle. Cyclin G1 is considered a major transcriptional target of TUMOR SUPPRESSOR PROTEIN P53 and is highly induced in response to DNA damage.

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

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

A family of basic helix-loop-helix transcription factors that control expression of a variety of GENES involved in CELL CYCLE regulation. E2F transcription factors typically form heterodimeric complexes with TRANSCRIPTION FACTOR DP1 or transcription factor DP2, and they have N-terminal DNA binding and dimerization domains. E2F transcription factors can act as mediators of transcriptional repression or transcriptional activation.

RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.

Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.

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

Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.

Substances that inhibit or prevent the proliferation of NEOPLASMS.

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

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

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

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

Histochemical localization of immunoreactive substances using labeled antibodies as reagents.

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

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

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

Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.

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

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

The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.

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

A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.

Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.

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

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

The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.

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

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

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

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

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

DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.

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

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

Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.

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

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

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

Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)

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

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

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

Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.

BENZOIC ACID amides.

The rate dynamics in chemical or physical systems.

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

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

Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.

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

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

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

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

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

Cyclin D-CDK subunit arrangement is dependent on the availability of competing INK4 and p21 class inhibitors. (1/120)

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)

Comparison of the effectiveness of adenovirus vectors expressing cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21(WAF1/CIP1) and p27KIP1 in inducing cell cycle arrest, apoptosis and inhibition of tumorigenicity. (2/120)

Cell cycle regulatory proteins are important candidates for therapeutic tumour suppressors. Adenovirus vectors were constructed to overexpress cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21(WAF1/CIP1) and p27KIP1 under the control of the murine cytomegalovirus immediate early gene promoter. These vectors directed the efficient expression of each of the cyclin kinase inhibitors and induced growth arrest, inhibited DNA synthesis, and prevented phosphorylation of the retinoblastoma protein (pRb) in cell lines expressing functional pRb. In pRb-deficient cells, expression of the cyclin kinase inhibitors was not effective in inhibiting DNA replication or growth arrest. Interestingly, three of the cyclin kinase inhibitors, p16, p18 and p27 were found to induce apoptotic death in transduced HeLa and A549 cells. When the vectors were tested for their ability to inhibit tumorigenicity in a polyomavirus middle T antigen model of murine breast carcinoma, expression of the cyclin kinase inhibitors resulted in a delay in tumour formation that varied from several weeks for the p19 expressing vector to greater than 25 weeks for the p27 expressing vector. When tumours were injected directly with the adenovirus vectors expressing the cyclin kinase inhibitors, only treatment with the vector expressing p16 resulted in a delay in tumour growth. (+info)

Role of PPARgamma in regulating a cascade expression of cyclin-dependent kinase inhibitors, p18(INK4c) and p21(Waf1/Cip1), during adipogenesis. (3/120)

Molecular mechanisms coupling growth arrest and cell differentiation were examined during adipogenesis. Data are presented that document a cascade expression of members of two independent families of cyclin-dependent kinase inhibitors that define distinct states of growth arrest during 3T3-L1 preadipocyte differentiation. Exit from the cell cycle into a pre-differentiation state of post-mitotic growth arrest was characterized by significant increases in p21 and p27. During onset of irreversible growth arrest associated with terminal differentiation, the level of p21 declined with a concomitant, dramatic increase in p18 and a sustained level of p27. The expression of p18 and p21, regulated at the level of protein and mRNA accumulation, was directly coupled to differentiation. Stable cell lines were engineered to express adipogenic transcription factors to examine the active role of trans-acting elements in regulating these cell cycle inhibitors. Ectopic expression of peroxisome proliferator-activated receptor (PPAR) gamma in non-precursor fibroblastic cell lines resulted in conversion to adipocytes and a coordinated increase in p18 and p21 mRNA and protein expression in a PPARgamma ligand-associated manner. These data demonstrate a role for PPARgamma in mediating the differentiation-dependent cascade expression of cyclin-dependent kinase inhibitors, thereby providing a molecular mechanism coupling growth arrest and adipocyte differentiation. (+info)

Down-regulation of the INK4 family of cyclin-dependent kinase inhibitors by tax protein of HTLV-1 through two distinct mechanisms. (4/120)

Tax oncoprotein of human T-cell leukemia virus type 1 (HTLV-1) affects multiple regulatory processes of infected cells through activation and repression of specific transcription and also through modulation of functions of cell cycle regulators. Previously, we found that Tax binds to p16ink4a, a member of the INK4 family of cyclin-dependent kinase inhibitors, and counteracts its inhibitory activity, resulting in cell cycle progression. In this study, we examined the effects of Tax on other members of the INK4 family and found that Tax can bind to p15ink4b similarly to p16ink4a, but not to p18ink4c and p19ink4d. Tax binding to p15ink4b inactivated its function and restored CDK4 kinase activity. Accordingly, Tax-expressing cells became resistant to p15ink4b-mediated growth arrest induced by TGFbeta. On the other hand, expression of p18ink4c was transcriptionally repressed by Tax through the E-box element of the promoter, which may contribute to the marked reduction of p18ink4c mRNA in HTLV-1-infected T-cells. These observations indicate that Tax suppresses the inhibitory activities of INK4 family members through two independent mechanisms: functional inhibition of two INK4 proteins and repression of expression of another INK4 protein. These effects may play roles in HTLV-1-induced deregulation of the cell cycle, possibly promoting cellular transformation. (+info)

An intrinsic timer that controls cell-cycle withdrawal in cultured cardiac myocytes. (5/120)

Developing cardiac myocytes divide a limited number of times before they stop and terminally differentiate, but the mechanism that stops their division is unknown. To help study the stopping mechanism, we defined conditions under which embryonic rat cardiac myocytes cultured in serum-free medium proliferate and exit the cell cycle on a schedule that closely resembles that seen in vivo. The culture medium contains FGF-1 and FGF-2, which stimulate cell proliferation, and thyroid hormone, which seems to be necessary for stable cell-cycle exit. Time-lapse video recording shows that the cells within a clone tend to divide a similar number of times before they stop, whereas cells in different clones divide a variable number of times before they stop. Cells cultured at 33 degrees C divide more slowly but stop dividing at around the same time as cells cultured at 37 degrees C, having undergone fewer divisions. Together, these findings suggest that an intrinsic timer helps control when cardiac myocytes withdraw from the cell cycle and that the timer does not operate by simply counting cell divisions. We provide evidence that the cyclin-dependent kinase inhibitors p18 and p27 may be part of the timer and that thyroid hormone may help developing cardiac myocytes stably withdraw from the cell cycle. (+info)

Cooperation of p27(Kip1) and p18(INK4c) in progestin-mediated cell cycle arrest in T-47D breast cancer cells. (6/120)

The steroid hormone progesterone regulates proliferation and differentiation in the mammary gland and uterus by cell cycle phase-specific actions. The long-term effect of progestins on T-47D breast cancer cells is inhibition of cellular proliferation. This is accompanied by decreased G(1) cyclin-dependent kinase (CDK) activities, redistribution of the CDK inhibitor p27(Kip1) among these CDK complexes, and alterations in the elution profile of cyclin E-Cdk2 upon gel filtration chromatography, such that high-molecular-weight complexes predominate. This study aimed to determine the relative contribution of CDK inhibitors to these events. Following progestin treatment, the majority of cyclin E- and D-CDK complexes were bound to p27(Kip1) and few were bound to p21(Cip1). In vitro, recombinant His(6)-p27 could quantitatively reproduce the effects on cyclin E-Cdk2 kinase activity and the shift in molecular weight observed following progestin treatment. In contrast, cyclin D-Cdk4 was not inhibited by His(6)-p27 in vitro or p27(Kip1) in vivo. However, an increase in the expression of the Cdk4/6 inhibitor p18(INK4c) and its extensive association with Cdk4 and Cdk6 were apparent following progestin treatment. Recombinant p18(INK4c) led to the reassortment of cyclin-CDK-CDK inhibitor complexes in vitro, with consequent decrease in cyclin E-Cdk2 activity. These results suggest a concerted model of progestin action whereby p27(Kip1) and p18(INK4c) cooperate to inhibit cyclin E-Cdk2 and Cdk4. Since similar models have been developed for growth inhibition by transforming growth factor beta and during adipogenesis, interaction between the Cip/Kip and INK4 families of inhibitors may be a common theme in physiological growth arrest and differentiation. (+info)

Distinct versus redundant properties among members of the INK4 family of cyclin-dependent kinase inhibitors. (7/120)

p16(INK4a), p15(INK4b), p18(INK4c) and p19(INK4d) comprise a family of cyclin-dependent kinase inhibitors and tumor suppressors. We report that the INK4 proteins share the ability to arrest cells in G1, and interact with CDK4 or CDK6 with similar avidity. In contrast, only p18 and particularly p19 are phosphorylated in vivo, and each of the human INK4 proteins shows unique expression patterns dependent on cell and tissue type, and differentiation stage. Thus, the INK4 proteins harbor redundant as well as non-overlapping properties, suggesting distinct regulatory modes, and diverse roles for the individual INK4 family members in cell cycle control, cellular differentiation, and multistep oncogenesis. (+info)

Limited overlapping roles of P15(INK4b) and P18(INK4c) cell cycle inhibitors in proliferation and tumorigenesis. (8/120)

Entry of quiescent cells into the cell cycle is driven by the cyclin D-dependent kinases Cdk4 and Cdk6. These kinases are negatively regulated by the INK4 cell cycle inhibitors. We report the generation of mice defective in P15(INK4b) and P18(INK4c). Ablation of these genes, either alone or in combination, does not abrogate cell contact inhibition or senescence of mouse embryo fibroblasts in culture. However, loss of P15(INK4b), but not of P18(INK4c), confers proliferative advantage to these cells and makes them more sensitive to transformation by H-ras oncogenes. In vivo, ablation of P15(INK4b) and P18(INK4c) genes results in lymphoproliferative disorders and tumor formation. Mice lacking P18(INK4c) have deregulated epithelial cell growth leading to the formation of cysts, mostly in the cortical region of the kidneys and the mammary epithelium. Loss of both P15(INK4b) and P18(INK4c) does not result in significantly distinct phenotypic manifestations except for the appearance of cysts in additional tissues. These results indicate that P15(INK4b) and P18(IKN4c) are tumor suppressor proteins that act in different cellular lineages and/or pathways with limited compensatory roles. (+info)

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

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

"Entrez Gene: CDKN2C cyclin-dependent kinase inhibitor 2C (p18, inhibits CDK4)". Ewing RM, Chu P, Elisma F, Li H, Taylor P, ... CDKN2C has been shown to interact with Cyclin-dependent kinase 4 and Cyclin-dependent kinase 6. GRCh38: Ensembl release 89: ... "Antitumour effect of cyclin-dependent kinase inhibitors (p16(INK4A), p18(INK4C), p19(INK4D), p21(WAF1/CIP1) and p27(KIP1)) on ... "Structure of the gene encoding the human cyclin-dependent kinase inhibitor p18 and mutational analysis in breast cancer". ...

https://en.wikipedia.org/wiki/CDKN2C

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 ...

https://en.wikipedia.org/wiki/Cyclin-dependent_kinase_6

... is a family of cyclin-dependent kinase inhibitors (CKIs). The members of this family (p16INK4a, p15INK4b, p18INK4c, ... Kovalev GI, Franklin DS, Coffield VM, Xiong Y, Su L (September 2001). "An important role of CDK inhibitor p18(INK4c) in ... Ortega S, Malumbres M, Barbacid M (March 2002). "Cyclin D-dependent kinases, INK4 inhibitors and cancer". Biochimica et ... cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4))". Atlas of genetics and cytogenetics in oncology and haematology. ...

https://en.wikipedia.org/wiki/INK4

... are specific inhibitors of the cyclin D-dependent kinases CDK4 and CDK6". Molecular and Cellular Biology. 15 (5): 2672-81. doi: ... Hirai H, Roussel MF, Kato JY, Ashmun RA, Sherr CJ (May 1995). "Novel INK4 proteins, p19 and p18, ... Cyclins function as regulators of cyclin-dependent kinases. Different cyclins exhibit distinct expression and degradation ... "Cyclin D- and E-dependent kinases and the p57(KIP2) inhibitor: cooperative interactions in vivo". Molecular and Cellular ...

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

1995). "Novel INK4 proteins, p19 and p18, are specific inhibitors of the cyclin D-dependent kinases CDK4 and CDK6". Mol. Cell. ... 2004). "Antitumour effect of cyclin-dependent kinase inhibitors (p16(INK4A), p18(INK4C), p19(INK4D), p21(WAF1/CIP1) and p27( ... Cyclin-dependent kinase 4 inhibitor D is an enzyme that in humans is encoded by the CDKN2D gene. The protein encoded by this ... "Entrez Gene: CDKN2D cyclin-dependent kinase inhibitor 2D (p19, inhibits CDK4)". Dehkordi, Shiva Kazempour; Walker, Jamie; Sah, ...

https://en.wikipedia.org/wiki/CDKN2D

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 ...

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

1995). "Novel INK4 proteins, p19 and p18, are specific inhibitors of the cyclin D-dependent kinases CDK4 and CDK6". Mol. Cell. ... "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. ...

https://en.wikipedia.org/wiki/Cyclin-dependent_kinase_4

"Evidence for different modes of action of cyclin-dependent kinase inhibitors: p15 and p16 bind to kinases, p21 and p27 bind to ... December 1994). "Growth suppression by p18, a p16INK4/MTS1- and p14INK4B/MTS2-related CDK6 inhibitor, correlates with wild-type ... "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 ... Cyclin-dependent kinase 4 inhibitor B also known as multiple tumor suppressor 2 (MTS-2) or p15INK4b is a protein that is ...

https://en.wikipedia.org/wiki/CDKN2B

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 ...

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

... cyclin-dependent kinase inhibitor p16 MeSH D12.776.624.776.355.300 - cyclin-dependent kinase inhibitor p18 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 p19 MeSH D12.776.624.776.355.500 - cyclin-dependent kinase inhibitor p21 MeSH D12.776.624.776 ... cyclin-dependent kinase 5 MeSH D12.776.167.200.067.900 - cyclin-dependent kinase 9 MeSH D12.776.167.200.580.500 - cdc2 protein ...

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

Kovalev GI, Franklin DS, Coffield VM, Xiong Y, Su L (September 2001). "An important role of CDK inhibitor p18(INK4c) in ... cyclin. In contrast to the stimulatory interaction with CD28, CD80 also regulates the immune system through an inhibitory ... activated protein kinase (MAPK), and the calcium‐calcineurin pathway. These changes initiate the production of numerous factors ... "The role of CD40 and CD80 accessory cell molecules in dendritic cell-dependent HIV-1 infection". Immunity. 1 (4): 317-25. doi: ...

https://en.wikipedia.org/wiki/CD80

Novel INK4 proteins, p19 and p18, are specific inhibitors of the cyclin D-dependent kinases CDK4 and CDK6. *H. Hirai, M. ... A small peptide inhibitor of DNA replication defines the site of interaction between the cyclin-dependent kinase inhibitor ... Structure of the cyclin-dependent kinase inhibitor p19Ink4d. *F. Luh, S. Archer, +8 authors. E. Laue ... Selective in vivo and in vitro effects of a small molecule inhibitor of cyclin-dependent kinase 4.. *R. Soni, T. Oreilly, +6 ...

https://www.semanticscholar.org/paper/Inhibition-of-pRb-phosphorylation-and-cell-cycle-by-F%C3%A5hraeus-Paramio/bfba3f77bdb9a8520398ffd7c0d56f99c1d1bb49

Cyclin-dependent kinase inhibitors (CDKIs) are proteins that bind to and inhibit the activity of CDKs. Two major classes of CDK ... inhibitors have been identified. The p16 family (p15, p16, p18 and p19) binds to and inhibits the activities of CDK4 and CDK6. ... Cyclin-dependent kinase 4 inhibitor A, CDK4I, p16-INK4, p16-INK4a, p16INK4A, CDKN-2A, CDKN2, Multiple tumor suppressor 1, MTS1 ... Lyophilized Cyclin-dependent kinase although stable at room temperature for 3 weeks, should be stored desiccated below -18°C. ...

https://www.prospecbio.com/cdkn2a_human

STRUCTURE OF CDK INHIBITOR P19INK4D. 1bi7. MECHANISM OF G1 CYCLIN DEPENDENT KINASE INHIBITION FROM THE STRUCTURE OF THE CDK6- ... SOLUTION STRUCTURE OF P18-INK4C, 21 STRUCTURES. 1d9s. TUMOR SUPPRESSOR P15(INK4B) STRUCTURE BY COMPARATIVE MODELING AND NMR ... MECHANISM OF G1 CYCLIN DEPENDENT KINASE INHIBITION FROM THE STRUCTURES CDK6-P19INK4D INHIBITOR COMPLEX. ... Drug Export Pathway of Multidrug Exporter AcrB Revealed by DARPin Inhibitors. 2jab. A designed ankyrin repeat protein evolved ...

https://smart.embl.de/smart/do_annotation.pl?DOMAIN=ANK&START=1130&END=1159&E_VALUE=7.59e-1&TYPE=SMART&BLAST=RKITPLMAAFRKGHVKVVRYLVKEVNQFPS

Cyclin Dependent Kinase Inhibitor 2C Cyclin Dependent Kinase Inhibitor p18 Cyclin-Dependent Kinase Inhibitor 2C INK4C Protein ... Cyclin Dependent Kinase Inhibitor 2C. Cyclin Dependent Kinase Inhibitor p18. Cyclin-Dependent Kinase Inhibitor 2C. INK4C ... Cyclin-Dependent Kinase Inhibitor p18 - Preferred Concept UI. M0240536. Scope note. An INK4 cyclin-dependent kinase inhibitor ... Cyclin-Dependent Kinase Inhibitor p18 Entry term(s). CDK6 Associated Protein p18 CDK6 Inhibitor, p18 CDK6-Associated Protein ...

https://decs.bvsalud.org/en/ths/resource/?id=50929

Protein Kinase C. 1. + 498. Cyclin-Dependent Kinase Inhibitor p18. 1. + 499. Galectin 3. 1. + ... Cyclin-Dependent Kinase Inhibitor p16. 2. + 173. O(6)-Methylguanine-DNA Methyltransferase. 2. + ... S-Phase Kinase-Associated Proteins. 1. + 590. Cyclin-Dependent Kinase 4. 1. + ...

https://lookfordiagnosis.com/results.php?symptoms=Melanoma%3B%20Malignant%20Melanoma&lang=1&parent=%2F&mode=F&therapy_ap=1

cyclin-dependent kinase inhibitor 2C (p18, inhibits CDK4). 0.045. Wwox. WW domain-containing oxidoreductase. 0.044. ... SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily d, member 1. 0.029. ... menage a trois homolog 1, cyclin H assembly factor (Xenopus laevis). 0.459. ...

http://imp.princeton.edu/predictions/process_ortho/fly-context-global/11882/?gene=145443

cyclin-dependent kinase inhibitor 2C (p18, inhibits CDK4). transcription factor 12. Image. ... a134c abp allelic ankyrin balb cdk6 cdnas chr congenic d2 dba g232a ifna inbred inefficient ink4c le multigenic mus p15 p16 p18 ... a134c abp allelic ankyrin balb cdk6 cdnas chr congenic d2 dba g232a ifna inbred inefficient ink4c le multigenic mus p15 p16 p18 ...

https://hagrid.dbmi.pitt.edu/wiki-pi/index.php/pair/view/1031/6938

p18 CDK6 Inhibitor use Cyclin-Dependent Kinase Inhibitor p18 p18 NF E2 Protein use MafK Transcription Factor ... p21 Cell Cycle Regulator use Cyclin-Dependent Kinase Inhibitor p21 p21 Cyclin Kinase Inhibitor use Cyclin-Dependent Kinase ... p27 CDK Inhibitor use Cyclin-Dependent Kinase Inhibitor p27 p27 Kip1 Protein use Cyclin-Dependent Kinase Inhibitor p27 ... p27, CDK Inhibitor use Cyclin-Dependent Kinase Inhibitor p27 p27Kip1 Protein use Cyclin-Dependent Kinase Inhibitor p27 ...

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

Among them, the cyclin-dependent kinase inhibitor 2A (CDKN2A or p16(INK4a)) gene has been shown to be frequently deleted or ... The CDKN2C (p18(INK4c)) gene is functionally related to CDKN2A. Moreover, mice with targeted disruption of CDKN2C alone or ... Genomic alterations of cyclin-dependent kinase inhibitors have been demonstrated in a variety of tumor types including brain ... combined CDKN2C and cyclin-dependent kinase inhibitor 1B (CDKN1B or p27(Kip1)), or CDKN2C and TP53 gene disruption develop ...

https://pesquisa.bvsalud.org/controlecancer/?lang=pt&q=au:Pinzer,+Thomas

31.. Tahara H, Smith AP, Gaz RD, Parathyroid tumor suppressor on 1p: Analysis of the p18 cyclin-dependent kinase inhibitor gene ... It has been proposed that parafibromin is an important modulator and regulator of gene expression dependent on the Hh-Wnt-NOTCH ... It suppresses cell cycle progression through the inhibition of the cyclin D1 promoter and c-myc oncogene (which may explain the ...

https://amjcaserep.com/abstract/full/idArt/936135

免疫組織化学 CpG Island *DNA変異分析 DNAメチル化プロモーター領域 RT-PCR法 SNPs *Cyclin-Dependent Kinase Inhibitor p18 *下垂体腺腫-成長ホルモン産生(遺伝学,診断) ヒト成人( ... Cyclin-dependent kinase inhibitors represented by the INK4 family comprising p16(INK4A), p15(INK4B), p18(INK4C), and p19(INK4D ... Adenoma / Adult / Aged / Aged, 80 and over / Cyclin-Dependent Kinase Inhibitor p18 / DNA Methylation / Down-Regulation / Female ... Further, blockage of phosphoinositide 3-kinase/Akt kinase with their specific inhibitors, LY294002

http://pub2.db.tokushima-u.ac.jp/ERD/person/82856/work-en.html

https://smart.embl.de/smart/do_annotation.pl?DOMAIN=ANK&START=155&END=183&E_VALUE=4.1e-2&TYPE=SMART&BLAST=DGFTPLAVALQQGHDQVVSLLLENDTKGK

https://smart.embl.de/smart/do_annotation.pl?DOMAIN=ANK&START=561&END=590&E_VALUE=4.85e-8&TYPE=SMART&BLAST=CGWTPLHEACNYGHLEIVRFLLDHGAAVDD

... cyclin-dependent kinases (Cdks), and cyclin-dependent kinase inhibitors (CdkIs) are essential for cell-cycle control in ... p18, p19, p21 and p27), called CdkIs, that bind to cyclins, Cdks, or cyclin-Cdk complexes. Cdk4 was originally called PSK-J3,2 ... cyclin-dependent kinases (Cdks), and cyclin-dependent kinase inhibitors (CdkIs) are essential for cell-cycle control in ... bind to cyclin-dependent kinases (Cdks), catalytic subunits, to form active cyclin-Cdk complexes. Cdk subunits by themselves ...

https://www.bdbiosciences.com/en-be/products/reagents/microscopy-imaging-reagents/immunofluorescence-reagents/purified-anti-human-cdk4-n-term.559693

Cyclin-Dependent Kinase Inhibitor p15, Cyclin-Dependent Kinase Inhibitor p18, DNA Methylation, Disease Progression, European ... Functional single nucleotide polymorphisms within the cyclin-dependent kinase inhibitor 2A/2B region affect pancreatic cancer ... Functional single nucleotide polymorphisms within the cyclin-dependent kinase inhibitor 2A/2B region affect pancreatic cancer ...

https://www.ceu.ox.ac.uk/publications/638502

Role of PPARgamma in regulating a cascade expression of cyclin-dependent kinase inhibitors, p18(INK4c) and p21(Waf1/Cip1), ... Phosphorylation of C/EBPbeta at a consensus extracellular signal-regulated kinase/glycogen synthase kinase 3 site is required ... was related to focal adhesion kinase (FAK) phosphorylation and epithelial-mesenchymal transition (EMT). It was involved in the ... Cell adaptive response to extracellular matrix density is controlled by ICAP-1-dependent beta1-integrin affinity, J. Cell Biol ...

https://aab.copernicus.org/articles/65/397/2022/aab-65-397-2022.html

... cyclin-cyclin-dependent kinase (cdk) machinery. As shown by immunoblot analysis, EGCG treatment of LNCaP and DU145 cells ... and INK4c/p18, (ii) down-modulation of the protein expression of cyclin D1, cyclin E, cdk2, cdk4, and cdk6, but not of cyclin ... This is the first systematic study showing the involvement of each component of cdk inhibitor-cyclin-cdk machinery during cell ... a hypothesis that EGCG-mediated cell cycle dysregulation and apoptosis is mediated via modulation of cyclin kinase inhibitor ( ...

http://thewallachfiles.com/green-tea-and-cancer-a-summary-of-the-evidence/

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

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

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

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

Inhibitors of mammalian G1 cyclin-dependent kinases. Sherr CJ, Roberts JM. Sherr CJ, et al. Genes Dev. 1995 May 15;9(10):1149- ... Differential post-transcriptional regulation of two Ink4 proteins, p18 Ink4c and p19 Ink4d. Forget A, Ayrault O, den Besten W, ... N-Myc and the cyclin-dependent kinase inhibitors p18Ink4c and p27Kip1 coordinately regulate cerebellar development. Zindy F, ... A New Cell-Cycle Target in Cancer - Inhibiting Cyclin D-Dependent Kinases 4 and 6. Sherr CJ. Sherr CJ. N Engl J Med. 2016 Nov ...

https://pubmed.ncbi.nlm.nih.gov/?term=Sherr+CJ&cauthor_id=7758941

The expression of three cyclin-dependent kinase inhibitors that regulate clonal expansion and postmitotic growth arrest during ... The expression of C/EBPβ, p18, p21, JUN, and ANGPTL4 presented similar alterations in subcutaneous adipose tissue of Lepob/ob ... adipocyte differentiation was also altered in obese subjects: p18 and p27 were downregulated, and p21 was upregulated. ...

https://bmcmedgenomics.biomedcentral.com/articles/10.1186/1755-8794-3-61/figures/5

Recombinant (E.Coli) Human Cyclin-Dependent Kinase Inhibitor 2A. > Recombinant (E.Coli, his tag) Human Tyrosine Kinase ErbB-2 ... Recombinant (E.Coli, GST tag) Epstein-Barr Virus (EBV/HHV-4) p18 ... Recombinant (E.Coli) Human Protein Kinase C Inhibitor Protein-1 ... Recombinant (E.Coli) c-AMP dependant Protein Kinase A regulatory subunit 2 alpha ... Recombinant (E.Coli) c-AMP dependant Protein Kinase A regulatory subunit-1 alpha ...

https://4adi.com/4adi/recombinant-e-coli-herpes-simplex-virus-2-gg-hsv-2-gg-22832-p.html

Recombinant (E.Coli) Human Cyclin-Dependent Kinase Inhibitor 2A. > Recombinant (E.Coli, his tag) Human Ephrin A1 ... Recombinant (E.Coli, GST tag) Epstein-Barr Virus (EBV/HHV-4) p18 ... Recombinant (E.Coli) c-AMP dependant Protein Kinase A catalytic ... Recombinant (E.Coli) c-AMP dependant Protein Kinase A regulatory subunit-1 alpha ... Recombinant (E.Coli) c-AMP dependant Protein Kinase A regulatory subunit 2 alpha ...

https://4adi.com/4adi/recombinant-e-coli-human-eotaxin-ccl11-his-tag-22390-p.html

We previously discovered that deletion of cell cycle inhibitors p16,sup,Ink4a,/sup, (p16) or p18,sup,Ink4c,/sup, (p18) is ... dependent. Inhibition of SIRT1 activity results in the phosphorylation of ER? in an AKT-dependent manner, and this activation ... The expression of the proliferation markers Cyclin E, c-Myc, and p45(Skp2) was differentially affected by ER?1 and ER?2 ... requires phosphoinositide 3-kinase activity. Phosphorylated ER? subsequently accumulates in the nucleus, where ER? binds DNA ER ...

https://www.omicsdi.org/dataset/biostudies/S-EPMC4792564

Functional collaboration between different cyclin-dependent kinase inhibitors suppresses tumor growth with distinct tissue ... P18 is a tumor suppressor gene involved in human medullary thyroid carcinoma and pheochromocytoma development. Wendy van Veelen ... Synergistic effect of oncogenic RET and loss of p18 on medullary thyroid carcinoma development. Wendy van Veelen, Carola J R ... In vitro and in vivo activity of cabozantinib (XL184), an inhibitor of RET, MET, and VEGFR2, in a model of medullary thyroid ...

https://cocites.com/coCitedArticles.cfm?pmid=26494382

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 ...

https://mdwiki.org/wiki/Proapoptotic

Cyclic Nucleotide Dependent-Protein Kinase *cyclin-dependent kinases(CDKs) *Cyclin-Dependent Protein Kinase ... Phosphoinositide 3-kinases (PI3-Ks) are a significant emerging course of drug goals,. immune Uncategorized bortezomib, p18 ... Sorafenib and Regorafenib, multi-kinase inhibitors for focusing on RAS/RAF/MEK/ERK signaling, have already been shown to boost ... Cell-permeable little molecule inhibitors be able to directly measure the phenotypic implications of inhibiting a kinase using ...

https://www.immune-source.com/tag/bortezomib/

Seidler, S. , Zimmermann, H. W., Bartneck, M., Trautwein, C., Tacke, F. (2010): Age-dependent alterations of monocyte subsets ... Cyclin E1 controls proliferation of hepatic stellate cells and is essential for liver fibrogenesis in mice.. Hepatology, 56 (3 ... High prevalence of Y-box protein-1/p18 fragment in plasma of patients with malignancies of different origin.. BMC Cancer, 14, ... Elevated serum levels of the mixed lineage kinase domain-like protein (MLKL) predict survival of patients during intensive care ...

https://sfbtrr57.de/projekte/p09/index.html

The cell cycle in mammalian cells is regulated by a series of cyclins and cyclin-dependent kinases (CDKs). (semanticscholar.org)
Inhibitors of mammalian G1 cyclin-dependent kinases. (nih.gov)

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

Cyclin-dependent kinase inhibitors (CDKIs) are proteins that bind to and inhibit the activity of CDKs. (prospecbio.com)

It is concluded that cyclin D:Cdk4/6 activity is required for early G1 phase cell cycle progression up to, but not beyond, activation of cyclin E:C DK2 complexes at the restriction point and is thus nonredundant with cyclin Cdk2 in late G1. (semanticscholar.org)
Inhibition of cyclin-dependent kinase 4 (Cdk4) by fascaplysin, a marine natural product. (semanticscholar.org)
Fascaplysin will prove to be a useful tool in studying the consequence of Cdk4 inhibition, especially in cells containing inactivated p16, and caused G1 arrest and prevented pRb phosphorylation at sites implicated as being specific for Cdk 4 kinase. (semanticscholar.org)
The p16 family (p15, p16, p18 and p19) binds to and inhibits the activities of CDK4 and CDK6. (prospecbio.com)

The PIKKs are proteins kinases that control cell development (mTORC1) or monitor genomic integrity (ATM, ATR, DNA-PK, and hSmg-1). (immune-source.com)

Synergistic effect of oncogenic RET and loss of p18 on medullary thyroid carcinoma development. (cocites.com)

P18 is a tumor suppressor gene involved in human medullary thyroid carcinoma and pheochromocytoma development. (cocites.com)

The p21 family (p21, p27, p28 and p57) can bind to broad range of CDK-cyclin complexes and inhibit their activities. (prospecbio.com)

PAPbeta, a protein that binds to and is phosphorylated by the non-receptor tyrosine kinase PYK2, contains several modular signaling domains including a pleckstrin homology domain, an SH3 domain, ankyrin repeats and an ARF-GAP domain. (embl.de)
Several derivatives of 5-aminoimidazole-4-carboxamide-1--d-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, were identified as transcriptional activators of the DDT gene. (tokushima-u.ac.jp)
2001). The course I PI3-Ks (p110, p110, p110, and p110) are turned on by tyrosine kinases or G protein-coupled receptors to create PIP3, which engages Bortezomib downstream effectors like the Akt/PDK1 pathway, the Tec family members kinases, as well Bortezomib as the Rho family members GTPases. (immune-source.com)

Furthermore, DDT mRNA levels were reduced in SGBS adipocytes treated with compound C, an AMPK inhibitor, suggesting involvement of AMPK in DDT transcription. (tokushima-u.ac.jp)
In conclusion, DDT transcription may be regulated in a cell-dependent manner, and were enhanced by AMPK activation in SGBS adipocytes through inhibiting the mTOR signaling. (tokushima-u.ac.jp)
A novel dual kinase function of the RET proto-oncogene negatively regulates activating transcription factor 4-mediated apoptosis. (cocites.com)

Role of cell cycle control and cyclin-dependent kinases in breast cancer. (semanticscholar.org)
Functional single nucleotide polymorphisms within the cyclin-dependent kinase inhibitor 2A/2B region affect pancreatic cancer risk. (ox.ac.uk)

Pituitary adenomas: role of cyclin-dependent kinase inhibitors, Springer, Oct. 2013. (tokushima-u.ac.jp)

N-Myc and the cyclin-dependent kinase inhibitors p18Ink4c and p27Kip1 coordinately regulate cerebellar development. (nih.gov)

Cell-type specific effects were also observed in the DDT gene expression of cells treated with AS1842856, a FOXO1 inhibitor. (tokushima-u.ac.jp)

2001). The PI3-K family members comprises 15 kinases with specific substrate specificities, appearance patterns, and settings of legislation (Katso et al. (immune-source.com)

CDK activity is modulated by the CDKIs p27 kip1 , p57 kip2 , p16 ink4A , p15 ink4B , p18 ink4C , and p19 ink4D . (medscape.com)
10. Alterations of the tumor suppressor genes CDKN2A (p16(INK4a)), p14(ARF), CDKN2B (p15(INK4b)), and CDKN2C (p18(INK4c)) in atypical and anaplastic meningiomas. (nih.gov)
11. Molecular analysis of a family of cyclin-dependent kinase inhibitor genes (p15/MTS2/INK4b and p18/INK4c) in non-small cell lung cancers. (nih.gov)
Antigen: KLH-conjugated synthetic peptide encompassing a sequence within the C-term region of human p18-INK4c. (glucagon-receptor.com)
Description: Cyclin-dependent kinase 4 inhibitor C (p18-INK4c) inhibits cell growth and proliferation with a correlated dependence on endogenous retinoblastoma protein RB. (glucagon-receptor.com)
p18-INK4c interacts strongly with CDK6, weakly with CDK4. (glucagon-receptor.com)
Growth arrest was not associated with upregulation of the CDK inhibitors p21(Waf1/Cip1), p18(ink4c) or p16(ink4a), but was associated with a decrease in reactive oxygen species (ROS). (nih.gov)

This protein has been shown to interact with CDK4 or CDK6, and prevent the activation of the CDK kinases, thus function as a cell growth regulator that controls cell cycle G1 progression. (nih.gov)
Aberrant gene expression, such as cyclin-dependent kinases CDK6 and cyclin-dependent kinase inhibitor p27, was found in the prenatal D4-treated mice. (researchsquare.com)
The INK4 gene family, including p15, p16, p18, and p19, bind to CDK4 and CDK6 and inhibit their kinase activities by interfering with their association with D-type cyclins. (researchsquare.com)
Cyclin D1, D2, or D3 proteins form complexes with Cyclin D dependent kinases (CDK4 or CDK6), which can then phosphorylate RB-1, and thereby decrease its ability to inhibit E2F transcription factors that increase expression of proteins involved in DNA synthesis. (biomedcentral.com)
Four INK4 inhibitors (p16INK4a, p15INK4b, p18INK4c, and p19INK4d) can bind to CDK4 or CDK6, thereby inhibiting Cyclin D activation of these kinases. (biomedcentral.com)

5. Deletions of the cyclin-dependent kinase inhibitor genes p16INK4A and p15INK4B in non-Hodgkin's lymphomas. (nih.gov)

Thirteen of 40 (33%) human myeloma cell lines do not express normal p18INK4c, with bi-allelic deletion of p18 in twelve, and expression of a mutated p18 fragment in one. (biomedcentral.com)

From NCBI Gene: The protein encoded by this gene is a member of the INK4 family of cyclin-dependent kinase inhibitors. (nih.gov)
To begin to identify cell cycle and cell death regulatory factors involved in antioxidant-induced growth arrest and PCD, we have studied colorectal carcinoma cells (CRCs) that differ in expression of the tumor suppressor protein p53, and of the cyclin-dependent kinase (CDK) inhibitor p21(Waf1/Cip1). (nih.gov)
PAPbeta, a protein that binds to and is phosphorylated by the non-receptor tyrosine kinase PYK2, contains several modular signaling domains including a pleckstrin homology domain, an SH3 domain, ankyrin repeats and an ARF-GAP domain. (embl.de)
Apart from a small fraction of cell lines and tumors that have inactivated the RB1 protein, it is not yet clear how other MM cell lines and tumors have become insensitive to the anti-proliferative effects of increased p18 expression. (biomedcentral.com)
Cyclin-dependent kinase 2 , also known as cell division protein kinase 2 , or Cdk2, is an enzyme that in humans is encoded by the CDK2 gene . (wikipedia.org)
[5] [6] The protein encoded by this gene is a member of the cyclin-dependent kinase family of Ser/Thr protein kinases . (wikipedia.org)
This protein kinase is highly similar to the gene products of S. cerevisiae cdc28 , and S. pombe cdc2, also known as Cdk1 in humans. (wikipedia.org)
This protein associates with and is regulated by the regulatory subunits of the complex including cyclin E or A . Cyclin E binds G1 phase Cdk2, which is required for the transition from G1 to S phase while binding with Cyclin A is required to progress through the S phase. (wikipedia.org)
Cdk2 becomes active when a cyclin protein (either A or E) binds at the active site located between the N and C lobes of the kinase. (wikipedia.org)
B3 Ku binds to the C-terminal region of DNA-PK (amino acids 3002-3850) near the protein kinase domain (Jin et al. (nih.gov)

2. Analysis of a family of cyclin-dependent kinase inhibitors: p15/MTS2/INK4B, p16/MTS1/INK4A, and p18 genes in acute lymphoblastic leukemia of childhood. (nih.gov)

1997) . c-Abl tyrosine kinase activity is stimulated in response to ionizing radiation, ara-C, camptothecin, or etoposide (Yuan et al. (nih.gov)
Selective compounds have been developed that target either the extracellular ligand-binding region of the EGFR (including a number of monoclonal antibodies [MAbs], immunotoxins, and ligand-binding cytotoxic agents) or the intracellular tyrosine kinase region (including various small-molecule inhibitors). (medscape.com)

20. Intragenic mutations of the p16(INK4), p15(INK4B) and p18 genes in primary non-small-cell lung cancers. (nih.gov)
Con frecuencia INK4B está inactivada por deleciones, mutaciones o hipermetilación en las NEOPLASIAS HEMATOLÓGICAS. (bvsalud.org)

1. Deletion of cyclin-dependent kinase 4 inhibitor genes P15 and P16 in non-Hodgkin's lymphoma. (nih.gov)
Bi-allelic deletion of p18, which appears to be a late progression event, has a prevalence of about 2% in 261 multiple myeloma (MM) tumors, but the prevalence is 6 to10% in the 50 tumors with a high expression-based proliferation index. (biomedcentral.com)

3. Loss of cyclin-dependent kinase inhibitor genes and chromosome 9 karyotypic abnormalities in human bladder cancer cell lines. (nih.gov)
6. Loss of chromosome arm 9p DNA and analysis of the p16 and p15 cyclin-dependent kinase inhibitor genes in human parathyroid adenomas. (nih.gov)
9. Review of alterations of the cyclin-dependent kinase inhibitor INK4 family genes p15, p16, p18 and p19 in human leukemia-lymphoma cells. (nih.gov)
12. Structural integrity of the cyclin-dependent kinase inhibitor genes, p15, p16 and p18 in myeloid leukaemias. (nih.gov)
13. Potential role for concurrent abnormalities of the cyclin D1, p16CDKN2 and p15CDKN2B genes in certain B cell non-Hodgkin's lymphomas. (nih.gov)
14. Alterations of the p15, p16,and p18 genes in osteosarcoma. (nih.gov)
C2 The Cyclin E and A genes (but not the Cyclin D gene) are strongly activated by E2F1 (DeGregori et al. (nih.gov)

It is a catalytic subunit of the cyclin-dependent kinase complex, whose activity is restricted to the G1-S phase of the cell cycle , where cells make proteins necessary for mitosis and replicate their DNA. (wikipedia.org)

Retroviral-mediated expression of exogenous p18 results in marked growth inhibition in three MM cell lines that express little or no endogenous p18, but has no effect in another MM cell line that already expresses a high level of p18. (biomedcentral.com)

[ 61 ] however, there are no reports of p18 alterations in human pituitary tumors. (medscape.com)

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

1997) . c-Abl-dependent phosphorylation of DNA-PK is stimulated by ionizing radiation (Kharbanda et al. (nih.gov)

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

Overexpression of pRb can increase the expression Cyclin D1 by an unknown mechanism (Watanabe et al. (nih.gov)

17. Absence of p18 mutations or deletions in lymphoid malignancies. (nih.gov)
B10 HMG1 or 2 compete with Ku for binding to DNA-PK and stimulate DNA-dependent kinase activity in vitro in the absence of Ku (Yumoto et al. (nih.gov)

Over-expression of transfected p18 restored coupled cell cycle arrest and differentiation in a B-lymphoblastoid cell line that was treated with IL-6. (biomedcentral.com)

In BCs, however, some physiological features like maximal firing rate, dynamic range, temporal response properties, recovery from post-stimulus depression, first spike latency (FSL) and encoding of sinusoid amplitude modulation undergo further maturation up to P18. (inno-406.info)

The ubiquitin/proteasome- dependent pathway plays an essential role in antigen presentation, cellular aging, apoptosis, and other major cellular processes. (nih.gov)

this interaction does not require c-Abl kinase activity. (nih.gov)

Paradoxically, although loss of p18 appears to contribute to increased proliferation of nearly 10% of MM tumors, most MM cell lines and proliferative MM tumors have increased expression of p18. (biomedcentral.com)

Paradoxically, 24 of 40 (60%) MM cell lines, and 30 of 50 (60%) MM tumors with a high proliferation index express an increased level of p18 RNA compared to normal bone marrow plasma cells, whereas this occurs in only five of the 151 (3%) MM tumors with a low proliferation index. (biomedcentral.com)

Inhibitors 2a, Supplementary Inhibitors S3 and Supplementary Inhibitors S1 demonstrate the results of this evaluation, which recommend that all through these three months, the a wave amplitude in T17M RHO CASP seven was enhanced from 166 478 in contrast with T17M RHO at P30 and P90, respectively. (kspinhibitors.com)

Anatomy7

Organisms2

Chemicals and Drugs72

Analytical, Diagnostic and Therapeutic Techniques and Equipment5

Phenomena and Processes29

Disciplines and Occupations1

Information Science3

Cyclin D-CDK subunit arrangement is dependent on the availability of competing INK4 and p21 class inhibitors. (1/120)

Comparison of the effectiveness of adenovirus vectors expressing cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21(WAF1/CIP1) and p27KIP1 in inducing cell cycle arrest, apoptosis and inhibition of tumorigenicity. (2/120)

Role of PPARgamma in regulating a cascade expression of cyclin-dependent kinase inhibitors, p18(INK4c) and p21(Waf1/Cip1), during adipogenesis. (3/120)

Down-regulation of the INK4 family of cyclin-dependent kinase inhibitors by tax protein of HTLV-1 through two distinct mechanisms. (4/120)

An intrinsic timer that controls cell-cycle withdrawal in cultured cardiac myocytes. (5/120)

Cooperation of p27(Kip1) and p18(INK4c) in progestin-mediated cell cycle arrest in T-47D breast cancer cells. (6/120)

Distinct versus redundant properties among members of the INK4 family of cyclin-dependent kinase inhibitors. (7/120)

Limited overlapping roles of P15(INK4b) and P18(INK4c) cell cycle inhibitors in proliferation and tumorigenesis. (8/120)

Cyclin-Dependent Kinase Inhibitor p27

Cyclin-Dependent Kinase Inhibitor p21

Cyclin-Dependent Kinases

Cyclins

Cell Cycle Proteins

Cyclin-Dependent Kinase Inhibitor p16

Cell Cycle

Tumor Suppressor Proteins

Microtubule-Associated Proteins

Cyclin-Dependent Kinase 2

Cyclin D1

Cyclin A

Cyclin E

Cell Proliferation

Cyclin-Dependent Kinase 4

CDC2-CDC28 Kinases

Apoptosis

Cyclin-Dependent Kinase Inhibitor p57

Cell Line, Tumor

Protein Kinase Inhibitors

Protein-Serine-Threonine Kinases

G1 Phase

Cyclin-Dependent Kinase 5

Cyclin B

Cyclin D

CDC2 Protein Kinase

Cyclin-Dependent Kinase Inhibitor Proteins

Cyclin C

Phosphorylation

Cyclin D3

Retinoblastoma Protein

Cyclin-Dependent Kinase 6

Cell Division

Enzyme Inhibitors

S Phase

Cyclin B1

Cyclin-Dependent Kinase Inhibitor p18

Tumor Suppressor Protein p53

Proto-Oncogene Proteins

Tumor Cells, Cultured

Signal Transduction

Cyclin D2

Cells, Cultured

Phosphatidylinositol 3-Kinases

Blotting, Western

E2F1 Transcription Factor

Cyclin A1

Protein Kinases

Purines

Transfection

Cell Line

Mitosis

Cyclin G

G2 Phase

Transcription Factor DP1

Mutation

Proliferating Cell Nuclear Antigen

Cyclin-Dependent Kinase Inhibitor p15

DNA-Binding Proteins

Cyclin G1

MAP Kinase Signaling System

Cyclin A2

E2F Transcription Factors

RNA, Messenger

Molecular Sequence Data

Carrier Proteins

Nuclear Proteins

Antineoplastic Agents

Transcription Factors

Base Sequence

Protein-Tyrosine Kinases

Calcium-Calmodulin-Dependent Protein Kinases

Immunohistochemistry

Cyclin-Dependent Kinase Inhibitor p19

S-Phase Kinase-Associated Proteins

src-Family Kinases

Enzyme Activation

Down-Regulation

Gene Expression Regulation

Protein Binding