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.

p57(Kip2) is degraded through the proteasome in osteoblasts stimulated to proliferation by transforming growth factor beta1. (1/288)

Cyclin-dependent kinase inhibitory proteins are negative regulators of the cell cycle. Although all the cyclin-dependent kinase inhibitory proteins may be involved in cell cycle control during a differentiation process, only p57(Kip2) is shown to be essential for embryonic development. However, the role of p57 in the control of the cell cycle is poorly understood. Using osteoblasts derived from the calvaria of rat fetus, we show that p57 is accumulated in cells starved by low serum. Cyclin-dependent kinase 2 activity was suppressed in these cells with a significant amount bound to p57. Treatment of the cells with transforming growth factor beta1 dramatically reduced the amount of p57, resulting in an activation of cyclin-dependent kinase 2 activity and the stimulation of cell proliferation. The decrease in p57 was inhibited by treating the cells with proteasome inhibitors, Z-Leu-Leu-Leu-aldehyde or lactacystin, but not with Z-Leu-Leu-aldehyde, which is an inhibitor of calpain, indicating that p57 is degraded through the proteasome pathway. p57 was also shown to be ubiquitinated in vitro. Because transforming growth factor beta1 not only stimulates the growth but also inhibits the differentiation of the cells in this system, our results may suggest a possible involvement of p57 in the control of osteoblastic cell proliferation and differentiation.  (+info)

Analysis of germline CDKN1C (p57KIP2) mutations in familial and sporadic Beckwith-Wiedemann syndrome (BWS) provides a novel genotype-phenotype correlation. (2/288)

Beckwith-Wiedemann syndrome (BWS) is a human imprinting disorder with a variable phenotype. The major features are anterior abdominal wall defects including exomphalos (omphalocele), pre- and postnatal overgrowth, and macroglossia. Additional less frequent complications include specific developmental defects and a predisposition to embryonal tumours. BWS is genetically heterogeneous and epigenetic changes in the IGF2/H19 genes resulting in overexpression of IGF2 have been implicated in many cases. Recently germline mutations in the cyclin dependent kinase inhibitor gene CDKN1C (p57KIP2) have been reported in a variable minority of BWS patients. We have investigated a large series of familial and sporadic BWS patients for evidence of CDKN1C mutations by direct gene sequencing. A total of 70 patients with classical BWS were investigated; 54 were sporadic with no evidence of UPD and 16 were familial from seven kindreds. Novel germline CDKN1C mutations were identified in five probands, 3/7 (43%) familial cases and 2/54 (4%) sporadic cases. There was no association between germline CDKN1C mutations and IGF2 or H19 epigenotype abnormalities. The clinical phenotype of 13 BWS patients with germline CDKN1C mutations was compared to that of BWS patients with other defined types of molecular pathology. This showed a significantly higher frequency of exomphalos in the CDKN1C mutation cases (11/13) than in patients with an imprinting centre defect (associated with biallelic IGF2 expression and H19 silencing) (0/5, p<0.005) or patients with uniparental disomy (0/9, p<0.005). However, there was no association between germline CDKN1C mutations and risk of embryonal tumours. No CDKN1C mutations were identified in six non-BWS patients with overgrowth and Wilms tumour. These findings (1) show that germline CDKN1C mutations are a frequent cause of familial but not sporadic BWS, (2) suggest that CDKN1C mutations probably cause BWS independently of changes in IGF2/H19 imprinting, (3) provide evidence that aspects of the BWS phenotype may be correlated with the involvement of specific imprinted genes, and (4) link genotype-phenotype relationships in BWS and the results of murine experimental models of BWS.  (+info)

CDKN1C expression in Beckwith-Wiedemann syndrome patients with allele imbalance. (3/288)

In this study, we have examined CDKN1C expression in BWS patients with allele imbalance (AI) affecting the 11p15 region. Two of two informative patients with AI, attributable to mosaic paternal isodisomy, exhibited reduced levels of CDKN1C expression in the liver and kidney, respectively, relative to expression levels in the equivalent tissues in normal controls. Although overall expression was reduced, some expression from the paternally derived CDKN1C allele was evident, consistent with incomplete paternal imprinting of the gene. One patient showed evidence of maternal allele silencing in addition to AI. These findings show for the first time that CDKN1C expression is reduced in BWS patients with AI and suggest that CDKN1C haploinsufficiency contributes to the BWS phenotype in patients with mosaic paternal isodisomies of chromosome 11.  (+info)

TGF-beta1-mediated hypertrophy involves inhibiting pRB phosphorylation by blocking activation of cyclin E kinase. (4/288)

When renal epithelial cells are exposed to epidermal growth factor-transforming growth factor-beta1 (EGF-TGF-beta1) the typical EGF-mediated hyperplastic growth response is converted to a hypertrophic growth response. Hypertrophy in this setting involves cell entrance into G(1), but arrest of cell cycle progression at the G(1)/S interface. Late G(1) arrest is mediated by retaining retinoblastoma protein (pRB) in its active, hypophosphorylated state. The present studies examine the mechanism by which pRB is retained in its active state. The results demonstrate that TGF-beta1-mediated conversion of hyperplasia to hypertrophy involves preventing activation of cdk2/cyclin E kinase but has no effect on cdk4(6)/cyclin D kinase activity. Preventing activation of cyclin E kinase is associated with 1) decreased abundance of cdk2/cyclin E complexes and 2) retention of p57(Kip2) in formed cdk2/cyclin E complexes. The development of hypertrophy does not involve regulation of either cdk2, cyclin E, or cdc25A protein abundances, or the abundance of p27(Kip1) or p21 in formed complexes.  (+info)

Spatial and temporal expression of p57(KIP2) during murine lens development. (5/288)

The expression patterns of p57(KIP2), an important cyclin-dependent kinase inhibitor in the lens, is investigated. This study shows that the expression of p57 mRNA throughout lens morphogenesis and growth correlates with lens cell withdrawal from the cell cycle (shown by changing patterns of BrdU incorporation) and the onset of lens fibre differentiation (shown by beta-crystallin expression). p57 expression at the early stages of fibre differentiation make it a useful marker for the initiation of this process.  (+info)

p57KIP2 expression and loss of heterozygosity during immortal conversion of cultured human mammary epithelial cells. (6/288)

We have uncovered a novel role for the cyclin-dependent kinase inhibitor, p57KIP2, during the immortalization of cultured human mammary epithelial cells (HMECs). HMECs immortalized after chemical carcinogen exposure initially expressed little or no telomerase activity, and their telomeres continued to shorten with passage. Cell populations whose mean terminal restriction fragment (TRF) length declined to < or = 3 kb exhibited slow heterogeneous growth and contained many nonproliferative cells. These conditionally immortal HMEC cultures accumulated large quantities of p57 protein. With continued passage, the conditionally immortal cell populations very gradually converted to a fully immortal phenotype of good uniform growth, expression of high levels of telomerase activity, and stabilization of telomere length. The fully immortal HMECs that grew well did not accumulate p57 in G0 or during the cell cycle. DNA and RNA analysis of mass populations and individual subclones of conditionally immortal HMEC line 184A1 showed that continued growth of conditionally immortal cells with critically short telomeres was repeatedly accompanied by loss of the expressed p57 allele and transient expression of the allele imprinted previously. Conditionally immortal 184A1 with mean TRF > 3 kb, infected with retroviruses containing the p57 gene, exhibited premature slow heterogeneous growth. Conversely, exogenous expression of human telomerase reverse transcriptase (hTERT), the catalytic subunit of telomerase, in 184A1 with mean TRF > 3 kb prevented both the slow heterogeneous growth phase and accumulation of p57 in cycling populations. These data indicate that in HMECs that have overcome replicative senescence, p57 may provide an additional barrier against indefinite proliferation. Overcoming p57-mediated growth inhibition in these cells may be crucial for acquisition of the unlimited growth potential thought to be critical for malignant progression.  (+info)

A human p57(KIP2) transgene is not activated by passage through the maternal mouse germline. (7/288)

Genomic imprinting results in expression of some autosomal genes from one parental allele only. Human chromosome 11p15, and the syntenic region on mouse distal chromosome 7, contain several imprinted genes, including p57 (KIP2) ( CDKN1C ) and IGF2. These two genes, which are separated by >700 kb, are both implicated in the pathogenesis of Beckwith-Wiedemann syndrome. We have shown previously that an Igf2/H19 transgene is expressed appropriately and can imprint at ectopic chromosomal locations. To investigate the p57 (KIP2) region, we similarly tested the imprinting and function of a 38 kb human genomic fragment containing the p57 (KIP2) gene in transgenic mice. This transgene showed appropriate tissue-specific expression and transgene copy number-dependent expression at ectopic sites. However, the levels of expression are reminiscent of that found for the paternal allele in humans (10%). There was no change in expression levels when the transgene was inherited from the maternal germline. These results suggest that the cis -elements required for enhanced expression of the maternally inherited p57 (KIP2) allele lie at a distance from the gene. This finding has important implications for the role of this gene in the human disease, in particular with respect to the translocation breakpoints identified in some patients.  (+info)

Mechanism for inactivation of the KIP family cyclin-dependent kinase inhibitor genes in gastric cancer cells. (8/288)

The mechanism for inactivation of the KIP family cyclin-dependent kinase inhibitor (CDKI) genes, the p21, p27, and p57 genes, in gastric cancer cells was tested by treating the cells with either the DNA demethylation agent, 5-aza-2'-deoxycytidine or the histone deacetylase inhibitor, n-butyric acid or trichostatin A. RNA expression of the gene was determined by reverse transcription PCR. The p21 gene was activated only by histone deacetylase inhibitor. The p57 gene was activated by histone deacetylase inhibitors in all of the gastric cancer cell lines and by 5-aza-2'-deoxycytidine in five of eight gastric cell lines. However, the p27 gene was not inactivated in gastric cancer cell lines. The methylation status of the promoter of the p21 and p57 genes was also tested by digestion with the methylation-sensitive restriction enzymes and a subsequent PCR. The promoter of the p21 gene has no methylation. The promoter of the p57 gene is, however, methylated in five of eight gastric cancer cell lines as expected from the result of the treatment with 5-aza-2'-deoxycytidine. Formation of the inactive chromatin through histone deacetylation seems to be the general mechanism for inactivation of both the p21 and the p57 genes in gastric cancer cells. Hypermethylation of promoter region seems to be an alternative pathway for inactivation of the p57 gene.  (+info)

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TY - JOUR. T1 - The two-domain hypothesis in Beckwith-Wiedemann syndrome. T2 - Autonomous imprinting of the telomeric domain of the distal chromosome 7 cluster. AU - Cerrato, Flavia. AU - Sparago, Angela. AU - Di Matteo, Ines. AU - Zou, Xiangang. AU - Dean, Wendy. AU - Sasaki, Hiroyuki. AU - Smith, Paul. AU - Genesio, Rita. AU - Bruggemann, Marianne. AU - Reik, Wolf. AU - Riccio, Andrea. PY - 2005/2/15. Y1 - 2005/2/15. N2 - A large cluster of imprinted genes is located on the mouse distal chromosome 7. This cluster is well conserved in humans and its dysregulation results in the overgrowth- and tumour-associated Beckwith-Wiedemann syndrome. Two imprinting centres (IC1 and IC2) controlling different sets of genes have been identified in the cluster, raising the hypothesis that the cluster is divided into two functionally independent domains. However, the mechanisms by which imprinting of genes in the IC2 domain (e.g. Cdkn1c and Kcnq1) is regulated have not been well defined, and recent evidence ...
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Fingerprint Dive into the research topics of The cyclin-dependent kinase inhibitor p21,sup,WAF1/Cip1,/sup, is an antiestrogen-regulated inhibitor of Cdk4 in human breast cancer cells. Together they form a unique fingerprint. ...
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J:96366 Cerrato F, Sparago A, Di Matteo I, Zou X, Dean W, Sasaki H, Smith P, Genesio R, Bruggemann M, Reik W, Riccio A, The two-domain hypothesis in Beckwith-Wiedemann syndrome: autonomous imprinting of the telomeric domain of the distal chromosome 7 cluster. Hum Mol Genet. 2005 Feb 15;14(4):503-11 ...
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E2-2 alteration influences cell cycle exit of progenitors in vivo. (A)E2-2 overexpression increased cell cycle exit (EdU+Ki67-/EdU+) among the progenitor cell
2017) Keywords: Biomarkers, Tumor Carcinoma, Squamous Cell Cell Transformation, Viral Cyclin-Dependent Kinase Inhibitor p16 DNA, Viral Humans In Situ Hybridization Neoplasm Proteins Oncogene Proteins, .... ...
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Beckwith-Wiedemann syndrome (BWS) is a well-studied human overgrowth disorder, associated with visceromegaly, exomphalos, and predisposition to Wilms tumor and other pediatric cancers. BWS is a clinical syndrome, not a single disorder. Phenotypic heterogeneity is prominent, and we now appreciate that this reflects an underlying molecular heterogeneity. The syndrome can be caused by various molecular defects, which lead to altered expression of certain imprinted genes on chromosome 11p15. Multiple studies have revealed striking epigenotype-phenotype correlations, in which exomphalos tracks with one type of imprinting defect, affecting the CDKN1C gene, while Wilms tumor predisposition tracks with a different imprinting defect, affecting the IGF2 and H19 genes. Here we review the clinical and molecular features of BWS and summarize the data from these recent investigations. We also review the fascinating association of BWS with twinning, and discuss preliminary studies suggesting an increased ...
Beckwith-Wiedemann syndrome (BWS) is a somatic overgrowth syndrome characterized by a variable incidence of congenital anomalies, including hemihyperplasia and renal malformations. BWS is associated with disruption of genomic imprinting and/or mutations in one or more genes encoded on 11p15.5, inclu …
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TY - JOUR. T1 - Molecular diagnosis of Beckwith-Wiedemann Syndrome using quantitative methylation-sensitive polymerase chain reaction. AU - Coffee, Bradford. AU - Muralidharan, Kasinathan. AU - Highsmith, William E.. AU - Lapunzina, Pablo. AU - Warren, Stephen T.. PY - 2006/10/1. Y1 - 2006/10/1. N2 - PURPOSE: Beckwith-Wiedemann Syndrome is caused by defects in imprinted gene expression at 11p15. Currently, quantitative Southern analysis using DNA methylation-sensitive restriction enzymes is used in molecular diagnosis of this syndrome. METHODS: We describe a rapid and highly quantitative test for assessing DNA methylation at 11p15 using sodium bisulfite treatment of genomic DNA coupled with quantitative TaqMan methylation-sensitive polymerase chain reaction. RESULTS: TaqMan MSP can assess DNA methylation at both differentially methylated region (DMR)1 and DMR2 at 11p15. In addition, by using TaqMan MSP we were able to determine the parent of origin of a duplication of 11p15 by quantification of ...
Despite its potential role as a tumor suppressor, p27 gene, a member of the Cip/Kip family of cyclin-dependent kinase inhibitor genes, has never been found mutated in human tumors. We investigated p27 protein expression in a series of 108 non-small cell lung cancers (57.4% stage 1, 16.7% stage 2, and 25.9% stage 3) to determine whether the lack or altered expression of this protein correlates with neoplastic transformation and/or progression. We performed immunohistochemistry and Western blot analysis of each specimen. We found that tumors expressing low to undetectable levels of p27 contained high p27 degradation activity. When we evaluated the outcome of the patients in relationship to p27 expression, we found p27 to be a prognostic factor correlating with the overall survival times (P = 0.0012).. The possibility of a simple assay, such as the immunohistochemical analysis of p27 expression on routinely formalin-fixed, paraffin-embedded specimens, has considerable value for the prognosis of ...
Features include: macroglossia, a large tongue which may cause breathing, feeding or speech difficulties; umbilical hernia or exomphalos; overgrowth, children are bigger than their contemporaries; hemihypertrophy, one side of the body grows more than the other; hypoglycaemia, low blood sugar as babies; characteristic facial appearance and indentations of the ears.
Recombinant human CDKN1B protein, fused to His-tag at N-terminus, was expressed in E. coli and purified by using conventional chromatography. MW: 24.2 kDa.
TABLE-US-00006 TABLE 6 THI + 2 + 4 + 5 + 7 Composite (Meta-THc) OG- OG- OG- OG- OG- 3116 @ 3116 @ 3116 @ 3116 @ 3116 @ 50 100 1 μg/ml 5 μg/ml 25 μg/ml μg/ml μg/ml Abl(H396P)(h) 91 88 73 55 50 Abl(M351T)(h) 100 87 62 50 38 Abl(Q252H)(h) 89 86 58 45 44 Abl(h) 98 85 65 41 49 Abl(m) 99 87 60 47 43 Abl(T315I)(h) 100 91 79 65 52 Abl(Y253F)(h) 93 90 75 54 51 ACK1(h) 122 112 97 102 82 ALK(h) 76 38 17 16 26 ALK4(h) 96 95 85 68 48 Arg(h) 94 91 68 52 42 Arg(m) 100 99 94 73 50 ARK5(h) 100 97 82 64 75 Aurora-A(h) 92 79 40 41 27 Axl(h) 97 99 83 77 60 Blk(m) 95 102 71 49 54 Bmx(h) 91 94 84 77 43 BrSK1(h) 95 90 71 47 51 BrSK2(h) 91 82 77 70 63 BTK(h) 99 97 64 44 28 CaMKI(h) 95 84 46 28 48 CaMKII(r) 97 106 89 69 63 CaMKIIβ(h) 94 99 85 52 34 CaMKIIγ(h) 107 103 94 92 134 CaMKIIδ(h) 103 97 84 83 84 CaMKIV(h) 107 108 95 75 58 CaMKIδ(h) 91 93 92 75 80 CDK1/cyclinB(h) 99 101 91 71 58 CDK2/cyclinA(h) 105 106 92 83 63 CDK2/cyclinE(h) 99 103 75 60 42 CDK3/cyclinE(h) 108 100 96 79 45 CDK5/p25(h) 102 89 84 77 72 ...
Harrison, T.A., Smith Adams, L.B., Moore, P.D., Perna, M.K., Sword, J.D.and Defoe, D. M.. Accelerated turnover of taste bud cells in mice deficient for the cyclin-dependent kinase inhibitor p27Kip1.BMC Neuroscience 2011, 12:34 ...
BCL6 interacts with the transcription factor Miz-1 to suppress the cyclin-dependent kinase inhibitor p21 and cell cycle arrest in germinal center B cells ...
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The p57(Kip2) cyclin-dependent kinase inhibitor (CDKi) has been implicated in embryogenesis, stem-cell senescence and pathologies, but little is known of its role in cell cycle control. Here, we show that p57(Kip2) is ...
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Beckwith-Wiedemann syndromeDefinitionBeckwith-Wiedemann syndrome (BWS) refers to a disorder of overgrowth. This condition is usually characterized by large body size (macrosomia), large tongue (macroglossia), enlarged internal organs (visceromegaly), the presence of an abdominal wall defect (umbilical hernia or omphalocele ), and low blood sugar in the newborn period (neonatal hypoglycemia). Source for information on Beckwith-Wiedemann Syndrome: Gale Encyclopedia of Genetic Disorders dictionary.
Cyclin-Dependent Kinase Inhibitor p27: A cyclin-dependent kinase inhibitor that coordinates the activation of CYCLIN and CYCLIN-DEPENDENT KINASES during the CELL CYCLE. It interacts with active CYCLIN D complexed to CYCLIN-DEPENDENT KINASE 4 in proliferating cells, while in arrested cells it binds and inhibits CYCLIN E complexed to CYCLIN-DEPENDENT KINASE 2.
Cyclin-Dependent Kinase Inhibitor p27: A cyclin-dependent kinase inhibitor that coordinates the activation of CYCLIN and CYCLIN-DEPENDENT KINASES during the CELL CYCLE. It interacts with active CYCLIN D complexed to CYCLIN-DEPENDENT KINASE 4 in proliferating cells, while in arrested cells it binds and inhibits CYCLIN E complexed to CYCLIN-DEPENDENT KINASE 2.
Beckwith-Wiedemann syndrome is an inherited growth disorder. Babies with this syndrome may have a range of symptoms. These symptoms may include large tongue (macroglossia), large organs (visceromegaly),
A collection of disease information resources and questions answered by our Genetic and Rare Diseases Information Specialists for Beckwith-Wiedemann syndrome
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ABERDEEN, S.D. - A South Dakota baby born with a tongue the size of an adults is smiling easily after a life-changing surgery. Little Paisley Morrison-Johnson, now 16 months old, was diagnosed with Beckwith-Wiedemann syndrome when she was born.
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Cyclin-dependent kinase inhibitor 1C, or p57, also affects corticogenesis. It has been shown the p57 induces cells to exit from ... The Cyclin-Dependent Kinase Inhibitor p57(Kip2) Regulates Cell Cycle Exit, Differentiation, and Migration of Embryonic Cerebral ... p57 is able to induce neuronal progenitor cells to start differentiating into highly specialized neurons in the cortex. However ... the mechanism by which p57 is able to affect such control is not yet known. Besides the ones listed above, there are several ...
In addition to p53 and Rb, cyclin dependent kinase inhibitors (CKIs), such as p21, p27, and p57, are also important for ... Immunoprecipitation kinase assays revealed that cyclin C has Rb kinase activity. Furthermore, unlike cyclins D and E, cyclin ... co-immunoprecipitation assays revealed that cyclin-dependent kinase 3 (cdk3) promotes G0 exit by forming a complex with cyclin ... Under normal conditions, the yeast cyclin-dependent kinase complex, Pho80-Pho85, inactivates the Pho4 transcription factor ...
"Cyclin D- and E-dependent kinases and the p57(KIP2) inhibitor: cooperative interactions in vivo". Molecular and Cellular ... Cyclins function as regulators of cyclin-dependent kinases. Different cyclins exhibit distinct expression and degradation ... are specific inhibitors of the cyclin D-dependent kinases CDK4 and CDK6". Molecular and Cellular Biology. 15 (5): 2672-81. doi: ... Meyerson M, Harlow E (Mar 1994). "Identification of G1 kinase activity for cdk6, a novel cyclin D partner". Molecular and ...
... (p57, Kip2), also known as CDKN1C, is a protein which in humans is encoded by the CDKN1C ... Cyclin-dependent kinase inhibitor 1C is a tight-binding inhibitor of several G1 cyclin/Cdk complexes and a negative regulator ... "Entrez Gene: CDKN1C cyclin-dependent kinase inhibitor 1C (p57, Kip2)". Matsuoka S, Edwards MC, Bai C, Parker S, Zhang P, ... Immuohistochemical stains for p57 can aid with the diagnosis of hydatidiform moles. Cyclin-dependent kinase inhibitor 1C has ...
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. ...
de Nooij JC; Graber KH; Hariharan IK (2001). "Expression of cyclin-dependent kinase inhibitor Dacapo is regulated by cyclin E ... activity involves Ago/Fbw7-mediated proteolytic degradation of cyclin E and direct inhibition by factors such as Dacapo and p57 ... Entry into endocycles involves modulation of mitotic and S-phase cyclin-dependent kinase (CDK) activity. Inhibition of M-phase ... "A Dominant Negative Mutant of Cyclin-Dependent Kinase A Reduces Endoreduplication but Not Cell Size or Gene Expression in Maize ...
... cyclin-dependent kinase inhibitor 1A, cyclin dependent kinase inhibitor 1A. External IDs. OMIM: 116899 MGI: 104556 HomoloGene: ... which is homologous to the other CIP/KIP CDK inhibitors p27 and p57.[6] Specifically it contains a Cy1 motif in the N-terminal ... 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 ...
CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... CDK4, CMM3, PSK-J3, cyclin-dependent kinase 4, cyclin dependent kinase 4. ... See also CDK inhibitor for inhibitors of various CDKs. Interactions[edit]. Cyclin-dependent kinase 4 has been shown to interact ... protein kinase activity. • kinase activity. • protein serine/threonine kinase activity. • cyclin-dependent protein serine/ ...
CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... "Identification of human cyclin-dependent kinase 8, a putative protein kinase partner for cyclin C". Proceedings of the National ... protein serine/threonine kinase activity. • cyclin-dependent protein serine/threonine kinase activity. ... The protein encoded by this gene is a member of the cyclin-dependent protein kinase (CDK) family. CDK8 and cyclin C associate ...
... has been shown to interact with: CDK9 CREB-binding protein Cyclin A1 Cyclin-dependent kinase inhibitor 1C EP300 PARP1 ... "The cell cycle-regulated B-Myb transcription factor overcomes cyclin-dependent kinase inhibitory activity of p57(KIP2) by ... The encoded protein is phosphorylated by cyclin A/cyclin-dependent kinase 2 during the S-phase of the cell cycle and possesses ... April 2001). "Cyclin A1 directly interacts with B-myb and cyclin A1/cdk2 phosphorylate B-myb at functionally important serine ...
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
"A current and comprehensive review of cyclin-dependent kinase inhibitors for the treatment of metastatic breast cancer". ... The cip/kip family includes the genes p21, p27 and p57. They halt the cell cycle in G1 phase by binding to and inactivating ... Two key classes of regulatory molecules, cyclins and cyclin-dependent kinases (CDKs), determine a cell's progress through the ... cyclin A, DNA polymerase, thymidine kinase, etc. Cyclin E thus produced binds to CDK2, forming the cyclin E-CDK2 complex, which ...
... 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 p15 MeSH D12.776.624.776.355.200 - cyclin-dependent kinase inhibitor p16 MeSH D12.776.624.776 ... cyclin-dependent kinase inhibitor p18 MeSH D12.776.624.776.355.400 - cyclin-dependent kinase inhibitor p19 MeSH D12.776.624.776 ... cyclin-dependent kinase 5 MeSH D12.776.167.200.067.900 - cyclin-dependent kinase 9 MeSH D12.776.167.200.580.500 - cdc2 protein ...
Cyclin-dependent kinase 4, Cyclin-dependent kinase inhibitor 1C, EP300, HDAC1, ID1, ID2, MDFI, MOS, Retinoblastoma protein, ... "Stabilization of MyoD by direct binding to p57(Kip2)". J. Biol. Chem. 275 (25): 18767-76. doi:10.1074/jbc.M907412199. PMID ... MyoD is inhibited by cyclin dependent kinases (CDKs). CDKs are in turn inhibited by p21. Thus MyoD enhances its own activity in ... Both MyoD and pRb are necessary for the repression of cyclin D1, but rather than acting directly on cyclin D1, they act on Fra- ...
... *Cyclin-dependent kinase inhibitor protein. *Cyclin-dependent kinase. *Cyclin. Lipid. *Phosphoinositide phospholipase C ... CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... cyclin E, A (Cdk2,1) cyclin A, B, B3 (Cdk1) H. sapiens cyclin D 1,2,3 (Cdk4, Cdk6) cyclin E (Cdk2) cyclin A (Cdk2, Cdk1) cyclin ... Cyclin A / CDK2 - active in S phase.. *Cyclin D / CDK4, Cyclin D / CDK6, and Cyclin E / CDK2 - regulates transition from G1 to ...
All these phases in the cell cycle are highly regulated by cyclins, cyclin-dependent kinases, and other cell cycle proteins. ... CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... Generation of pressure is dependent on formin-mediated F-actin nucleation[71] and Rho kinase (ROCK)-mediated myosin II ... This can occur when cells become overcrowded (density-dependent inhibition) or when they differentiate to carry out specific ...
CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... Finally, the Akt protein kinase promotes cell survival through two pathways. Akt phosphorylates and inhibits Bad (a Bcl-2 ... 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 ...
CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... April 2010). "Apoptosis induced by Oropouche virus infection in HeLa cells is dependent on virus protein expression". Virus Res ... Finally, the Akt protein kinase promotes cell survival through two pathways. Akt phosphorylates and inhibits Bas (a Bcl-2 ... Cyclin. *A (A1, A2). *B (B1, B2, B3). *D (D1, D2, D3) ... Using these inhibitors it was discovered that cells can die ...
CDKN2C, INK4C, p18, p18-INK4C, cyclin-dependent kinase inhibitor 2C, cyclin dependent kinase inhibitor 2C. ... CDK inhibitor. *دورة الخلية (p14arf/p16, CDKN2B, CDKN2C, CDKN2D). *دورة الخلية (p21, p27, p57) ... CDKN2C‏ (Cyclin dependent kinase inhibitor 2C) هوَ بروتين يُشَفر بواسطة جين CDKN2C في الإنسان.[1][2][3] ... "Entrez Gene: CDKN2C cyclin-dependent kinase inhibitor 2C (p18, inhibits CDK4)". مؤرشف من الأصل في 05 ديسمبر 2010.. الوسيط , ...
CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... Cyclin. *A (A1, A2). *B (B1, B2, B3). *D (D1, D2, D3) ... CDK-activating kinase. ... "Predominant suppression of apoptosome by inhibitor of apoptosis protein in non-small cell lung cancer H460 cells: therapeutic ...
GTP-dependent protein binding. • GTPase activity. • mitogen-activated protein kinase kinase kinase binding. • protein binding. ... CDK inhibitor. *INK4a/ARF (p14arf/p16, p15, p18, p19). *cip/kip (p21, p27, p57) ... Cyclin. *A (A1, A2). *B (B1, B2, B3). *D (D1, D2, D3) ... "The MAP kinase kinase kinase MLK2 co-localizes with activated ... protein kinase binding. • nucleotide binding. • GTP binding. • identical protein binding. Cellular component. • cytoplasm. • ...
Cyclin-dependent kinase 4,[30][31]. *Cyclin-dependent kinase inhibitor 1C,[32] ... "Stabilization of MyoD by direct binding to p57(Kip2)". J. Biol. Chem. 275 (25): 18767-76. doi:10.1074/jbc.M907412199. PMID ... MyoD is inhibited by cyclin dependent kinases (CDKs). CDKs are in turn inhibited by p21. Thus MyoD enhances its own activity in ... Both MyoD and pRb are necessary for the repression of cyclin D1, but rather than acting directly on cyclin D1, they act on Fra- ...
... negative regulation of cyclin-dependent protein serine/threonine kinase activity, negative regulation of mitotic cell cycle, ... Cyclin-dependent kinase inhibitor 1C (P57, Kip2)Imported. Automatic assertion inferred from database entriesi ... tr,Q6IQT7,Q6IQT7_DANRE Cyclin-dependent kinase inhibitor 1C (P57, Kip2) OS=Danio rerio OX=7955 GN=cdkn1ca PE=2 SV=1 ... Cyclin-dependent kinase inhibitor 1CaImported. Automatic assertion inferred from database entriesi ...
cyclin-dependent kinase inhibitor 1C (P57). Synonyms: CDKI, Kip2, p57Kip2. Gene nomenclature, locus information, and GO, OMIM, ... OMIM: BECKWITH-WIEDEMANN SYNDROME; BWS, PREECLAMPSIA/ECLAMPSIA 1; PEE1, CYCLIN-DEPENDENT KINASE INHIBITOR 1C; CDKN1C, 614732* ...
P57(KIP2). Cyclin-dependent kinase inhibitor 1c. PI3K. Phosphatidylinositol 3-kinase. ProSAP2 (SHANK3). Proline-rich synapse- ...
cyclin-dependent kinase inhibitor 1C (p57, Kip2). *cyclin-dependent kinase inhibitor p57 ... p57(Kip2)) analysis in Beckwith-Wiedemann syndrome (BWS) patients: Genotype-phenotype correlations, novel mutations, and ... cyclin-dependent kinase inhibitor 1C. * ... cyclin dependent kinase inhibitor 1C To use the sharing ...
Cyclin-Dependent Kinase Inhibitor p57 / metabolism* * Homeodomain Proteins / genetics * Homeodomain Proteins / metabolism* ... Transcriptional profile analysis of E14.5 Arx-ablated cortices compared with control revealed that CDKN1C, an inhibitor of cell ...
Cyclin-Dependent Kinase Inhibitor p57 * Nuclear Proteins ... p57(KIP2)). It was hypothesized that genotypic and epigenotypic ...
Cdkn1c-; p57+/-m; p57-; p57KIP2. Gene Symbol and Name. Cdkn1c, cyclin-dependent kinase inhibitor 1C (P57). ... Also Known As:p57-. These Cdkn1c knock-out mice exhibit altered cell proliferation and differentiation, and display several ... When using the p57- mouse strain in a publication, please cite the originating article(s) and include JAX stock #003336 in your ... A targeting construct that removed exons 1 and 2 (87% of the p57KIP2 coding region) was introduced into AB2.1 embryonic stem ...
Cyclin-dependent kinase inhibitor 1C (p57, Kip2), also known as CDKN1C, is a protein which in humans is encoded by the CDKN1C ... Cyclin-dependent kinase inhibitor 1C is a tight-binding inhibitor of several G1 cyclin/Cdk complexes and a negative regulator ... "Entrez Gene: CDKN1C cyclin-dependent kinase inhibitor 1C (p57, Kip2)". Matsuoka S, Edwards MC, Bai C, Parker S, Zhang P, ... Immuohistochemical stains for p57 can aid with the diagnosis of hydatidiform moles. Cyclin-dependent kinase inhibitor 1C has ...
... cyclin-dependent kinase inhibitor 1B; p57, cyclin-dependent kinase inhibitor 1C; c-Kit, kit oncogene; Myocd, myocardin; MRTF, ... The serine/threonine kinase Akt (also known as protein kinase B)/phosphoinositide-3 kinase (PI3K) signaling pathway plays a key ... NF-kappaB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses. Proc ... Ca2+/calmodulin kinase II-dependent regulation of atrial myocyte late Na+ current, Ca2+ cycling and excitability: a ...
... produces protein cyclin-dependent kinase inhibitor 1C (p57, Kip2) P57, kinase inhibitory protein 2 of cyclins (p57) ... CMV-p57 TypeStrain=False Application: in another host, ... cyclin-dependent kinase inhibitor 1C (p57, Kip2)(P57, kinase ... produces protein cyclin-dependent kinase inhibitor 1C (p57, Kip2) P57, kinase inhibitory protein 2 of cyclins (p57) ... CMV-p57 (ATCC® 63340™) Organism: Mus musculus, mouse / Clone Type: Clone / Depositors: SJ Elledge ...
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. ...
The invention provides methods for assessing the efficacy of histone deacetylase inhibitors using biomarkers which can be used ... cyclin-dependent kinase. NM_000076. CDKN1C. inhibitor 1C (p57, Kip2). 2.8. superoxide dismutase 2,. AL050388;. SOD2. ... These include induction of cell cycle inhibitors such as the cyclin-dependent kinase inhibitor p21, induction of proapoptotic ... Plasminogen Activator Inhibitor-1 Inhibitors And Methods Of Use Thereof To Modulate Lipid Metabolism. January, 2009. Lawrence ...
tracked down the molecule that makes up this mitogen-dependent intracellular timer. The cyclin-dependent kinase inhibitor p57 ... Overexpression of p57Kip2 slowed the proliferation rate of OPCs in vitro to various degrees, depending on the availability of ... Thus, p57Kip2 fulfills the criteria for the primary component of this cellular clock, informing the cells when to abandon the ... Buildup of p57Kip2 also triggered expression of early gene markers of myelination. When the authors knocked down expression of ...
The activation of specific cyclin-dependent kinases (CDK) promotes cell proliferation. The cyclin-CDK complex is negatively ... regulated by CDK inhibitors p21, p27, and p57. Podocyte injury induces the loss of function of p27 and p57, resulting in ... The increased production of TGF-β might induce the expression of the integrin-linked kinase (ILK), a protein which is related ... Y. S. Kang, Y. Li, C. Dai, L. P. Kiss, C. Wu, and Y. Liu, "Inhibition of integrin-linked kinase blocks podocyte epithelial- ...
The cyclin-dependent kinase inhibitor p57Kip2 mediates proliferative actions of PTHrP in chondrocytes. ... The cyclin-dependent kinase inhibitor p57Kip2 mediates proliferative actions of PTHrP in chondrocytes. ... Because the bone phenotype of mice lacking the cyclin-dependent kinase inhibitor p57Kip2 is the opposite of the PTHrP-null ... We generated p57/PTHrP-null embryos, which showed partial rescue of the PTHrP-null phenotype. There was reversal of the loss of ...
Cyclin-Dependent Kinase Inhibitor 1C (CDKN1C) is a tumor suppressor; a protein involved in the regulation of cell division. ... Because it is a strong, tight inhibitor of several G1 cyclin/CDK complexes, this protein is a negative regulator of cell ...
Invitrogen Anti-p57 Kip2 Monoclonal (3E3), Catalog # MA5-15720. Tested in Western Blot (WB) applications. This antibody reacts ... Cyclin-dependent kinase inhibitor 1C; cyclin-dependent kinase inhibitor 1C (p57, Kip2); Cyclin-dependent kinase inhibitor p57; ... Cite p57 Kip2 Monoclonal Antibody (3E3). The following product was used in this experiment: p57 Kip2 Monoclonal Antibody (3E3) ... negative regulation of kinase activity multicellular organism growth negative regulation of phosphorylation neuron maturation ...
Cyclin-dependent kinase inhibitor 1C (p57, Kip2). NM_000076. NM_001122630. NM_001122631. Gene Info. ... Cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4). NM_078487. NM_004936. 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. ...
2007) The cyclin-dependent kinase inhibitors p57 and p27 regulate neuronal migration in the developing mouse neocortex. J Biol ... 2004) The cyclin-dependent kinase inhibitor p57(Kip2) mediates proliferative actions of PTHrP in chondrocytes. J Clin Invest ... Here, we report the discovery of such a molecule, the cyclin-dependent kinase inhibitor p57Kip2 (Cdkn1c). We show in vitro that ... 2001) Cyclin-dependent kinase inhibitors in the development of the central nervous system. Cell Growth Differ 12:387-396. ...
Cyclin-dependent Kinase Inhibitor p57KIP2 in Soft Tissue Sarcomas and Wilms Tumors ... Cyclin-dependent Kinase Inhibitor p57KIP2 in Soft Tissue Sarcomas and Wilms Tumors ... Cyclin-dependent Kinase Inhibitor p57KIP2 in Soft Tissue Sarcomas and Wilms Tumors ... Cyclin-dependent Kinase Inhibitor p57KIP2 in Soft Tissue Sarcomas and Wilms Tumors ...
Cyclin dependent kinase inhibitor 1C (CDKN1C); Cyclin dependent kinase inhibitor p57; KIP2; p57; p57Kip2 ... Cloning of p57, a cyclin-dependent kinase inhibitor with unique domain structure and tissue distribution. Genes Dev. 9: 639-649 ... p57Kip2 is a potent tight-binding inhibitor of several G1 cyclin complexes, and is a negative regulator of cell proliferation. ... Anti-p57 has been used as an aide in identification of complete hydatidiform mole (CHM) (no nuclear labeling of ...
Oligodendrocyte precursor differentiation is perturbed in the absence of the cyclin-dependent kinase inhibitor p27Kip1. Genes ... A crucial role for p57(Kip2) in the intracellular timer that controls oligodendrocyte differentiation. J Neurosci. 2007;27(23): ... Age-dependent epigenetic control of differentiation inhibitors is critical for remyelination efficiency. Nat Neurosci. 2008;11( ... Olinone, an inhibitor the team developed against these bromodomains, increased OPC differentiation in cultured cells. They plan ...
Li Y, Wang D, Zhang H, Wang C, Dai W, et al.. (2013) P21-Activated Kinase 4 Regulates the Cyclin-Dependent Kinase Inhibitor P57 ... The mRNA levels of USP22, BMI-1, p14ARF, c-Myc and cyclin D2, as well as that of the internal standard β-actin, were measured ... The results showed that USP22 was able to promote an increase in the endogenous concentration of c-Myc and cyclin D2 mRNA ( ... We examined the transcriptional relationship in the BMI-1, p14ARF, c-Myc and cyclin D2 expression by quantitative real-time PCR ...
Cloning of p57KIP2, a cyclin-dependent kinase inhibitor with unique domain structure and tissue distribution. Genes Dev, 9(6): ... Cloning of p27kip1, a cyclin-dependent kinase inhibitor and a potential mediator of extracellular antimitogenic signals. Cell, ... The p21 Cdkinteracting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases. Cell, 75(4):805-816. https://doi.org/ ... p27, a novel inhibitor of G1 cyclin-Cdk protein kinase activity, is related to p21. Cell, 78(1):67-74. https://doi.org/10.1016/ ...
cyclin-dependent kinase inhibitor 1C , cyclin-dependent kinase inhibitor p57 , cyclin-dependent kinase inhibitor 1C (p57, Kip2 ... Cyclin-Dependent Kinase Inhibitor 2B (p15, Inhibits CDK4) ELISA Kits * Cyclin-Dependent Kinase Inhibitor 2C (p18, Inhibits CDK4 ... Cyclin-Dependent Kinase 5, Regulatory Subunit 2 (p39) ELISA Kits * Cyclin-Dependent Kinase 5, Regulatory Subunit 1 (p35) ELISA ... cyclin-dependent kinase inhibitor 1Ca (cdkn1ca) ELISA Kit * cyclin-dependent kinase inhibitor 1C (P57) (Cdkn1c) ELISA Kit ...
Cyclin D- and E-dependent kinases and the p57(KIP2) inhibitor: cooperative interactions in vivo. Mol Cell Biol 1999; 19: 353-63 ... a pan cyclin-dependent kinase inhibitor, which has been shown to bind to and directly inhibit cyclin B1-CDC2 kinase, CDK2, CDK4 ... The universal CDI inhibitor Kip2 (p57, CDKN1C), which inhibits all of the G1 kinases (CDK2, CDK4, and CDK6), is 5-fold reduced ... The cyclin D-CDK4/6 for G1 progression ( 31), cyclin E-CDK2 for G1-S transition, cyclin A-CDK2 for S-phase progression ( 32), ...
2004). The cyclin-dependent kinase inhibitor p57 (Kip2) mediates proliferative actions of PTHrP in chondrocytes. J. Clin. ... 2000). Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1. Science 287, 664 ... and double-stranded RNA-activated protein kinase-likeendoplasmic reticulum kinase (PERK) in transcription during the mammalian ... H) Runx2-dependent transactivation of pATF6 gene was dramatically reduced when the Runx2-binding site was mutated (Mut1). The ...
These genes encode proteins called insulin-like growth factor-II (IGF-II) and p57kip2. The latter is a cyclin-dependent kinase ... while that known as CDKN1C p57kip2 is expressed from the maternally derived copy of the gene, and is a growth inhibitor. ... She said: "So we decided to do some simple experiments to see if IGF2 could affect expression of p57kip2 in a dose-dependent ... Ferguson-Smith said, "We found that p57kip2 expression was down-regulated in a dose-dependent manner in response to IGF-II." ...
CDKN1C encodes the protein p57KIP2, a member of the cyclin-dependent kinase inhibitor family which acts to negatively regulate ... A maternally inherited pathogenic variant in CDKN1C leading to increased stability of cyclin-dependent kinase inhibitor 1C was ... Oppositely imprinted genes p57(Kip2) and igf2 interact in a mouse model for Beckwith-Wiedemann syndrome. Genes Dev. 1999;13: ... Upregulation of Igf2 expression and downregulation of Cdkn1c (p57Kip2) result in phenotypes analogous to BWS in mouse models [ ...
... p57, Kip2)) for WB, IHC-Wm. Anti-Cdkn1c pAb (GTX54219) is tested in Zebrafish samples. 100% Ab-Assurance. ... cyclin-dependent kinase inhibitor 1C (p57, Kip2). Synonyms. cb961 Antibody , cdkn1c Antibody , cyclin-dependent kinase ...
  • A targeting construct that removed exons 1 and 2 (87% of the p57 KIP2 coding region) was introduced into AB2.1 embryonic stem cells. (jax.org)
  • Cyclin-dependent kinase inhibitor 1C (p57, Kip2), also known as CDKN1C, is a protein which in humans is encoded by the CDKN1C imprinted gene. (wikipedia.org)
  • The following product was used in this experiment: p57 Kip2 Monoclonal Antibody (3E3) from Thermo Fisher Scientific, catalog # MA5-15720, RRID AB_11000208. (thermofisher.com)
  • Here, we report the discovery of such a molecule, the cyclin-dependent kinase inhibitor p57 Kip2 (Cdkn1c). (jneurosci.org)
  • We show in vitro that all daughters of a clone of OPCs express similar levels of p57 Kip2 , that p57 Kip2 levels increase over time in proliferating OPCs, and that p57 Kip2 levels regulate how many times an OPC can divide before differentiating. (jneurosci.org)
  • CyclinE-cdk2 complex formation is inhibited by members of the Cip/Kip family of cyclin-dependent kinase inhibitor proteins ( Cunningham and Roussel, 2001 ), and all three members of this family, p21 Cip1 , p27 Kip1 , and p57 Kip2 , have been implicated in regulating various stages of OL differentiation. (jneurosci.org)
  • We report here that p57 Kip2 is an important component of the OPC timer as well as the mechanism that couples the regulation of OPC proliferation and differentiation. (jneurosci.org)
  • A gene known as IGF2 is expressed from the paternally derived copy of the gene, and is a growth promoter, while that known as CDKN1C p57 kip2 is expressed from the maternally derived copy of the gene, and is a growth inhibitor. (bioworld.com)
  • These genes encode proteins called insulin-like growth factor-II (IGF-II) and p57 kip2 . (bioworld.com)
  • Ferguson-Smith and her team decided to investigate further and results are described in the May 9, 2000, Proceedings of the National Academy of Sciences in a paper titled "Increased IGF-II protein affects p57 kip2 expression in vivo and in vitro: Implications for Beckwith-Wiedemann syndrome. (bioworld.com)
  • Other studies examined the possible genetic causes of the familial Beckwith-Wiedemann cases, and found that about 5 percent of these had mutations in their p57 kip2 gene. (bioworld.com)
  • One possibility is that they are interacting in the same pathway and that overexpression of IGF2 might be affecting p57 kip2 in some way. (bioworld.com)
  • Mouse models also provided clues to the function of IGF-II and p57 kip2 . (bioworld.com)
  • Those that have mutations in p57 kip2 also have some but not all of the features of the disease. (bioworld.com)
  • She said: "So we decided to do some simple experiments to see if IGF2 could affect expression of p57 kip2 in a dose-dependent manner. (bioworld.com)
  • We show that expression of p57 Kip2 , a potent tight-binding inhibitor of several G 1 cyclin-cyclin-dependent kinase (Cdk) complexes, increases markedly during C2C12 myoblast differentiation. (asm.org)
  • We examined the effect of p57 Kip2 on the activity of the transcription factor MyoD. (asm.org)
  • In addition, p57 Kip2 , p21 Cip1 , and p27 Kip1 but not p16 Ink4a induced an increased level of MyoD protein, and we show that MyoD, an unstable nuclear protein, was stabilized by p57 Kip2 . (asm.org)
  • Forced expression of p57 Kip2 correlated with hypophosphorylation of MyoD in C2C12 myoblasts. (asm.org)
  • Furthermore, phosphorylation of MyoD by purified cyclin E-Cdk2 complexes was inhibited by p57 Kip2 . (asm.org)
  • In addition, the NH2 domain of p57 Kip2 necessary for inhibition of cyclin E-Cdk2 activity was sufficient to inhibit MyoD phosphorylation and to stabilize it, leading to its accumulation in proliferative myoblasts. (asm.org)
  • Taken together, our data suggest that repression of cyclin E-Cdk2-mediated phosphorylation of MyoD by p57 Kip2 could play an important role in the accumulation of MyoD at the onset of myoblast differentiation. (asm.org)
  • p21 Cip1 , p27 Kip1 , and p57 Kip2 , members of the other family of inhibitors, the Cip/Kip family, have the ability to inhibit all G 1 /S-phase cyclin-Cdk complexes ( 19 , 49 , 56 ). (asm.org)
  • p57 Kip2 is also a tight-binding inhibitor of cyclin A/E-Cdk2 and cyclin D-Cdk4/Cdk6 complexes and a negative regulator of cell proliferation ( 25 , 33 ). (asm.org)
  • The expression pattern of p57 mRNA in various adult human tissues indicates that its distribution is more restricted than that of p21 Cip1 and p27 Kip1 ( 25 , 33 ), suggesting that p57 Kip2 has an important role during development ( 61 , 62 ). (asm.org)
  • These genes include CDKN1C (also known as p57 KIP2 ), KCNQ1 ( KVLQT1 ), SLC22A1L , and TSSC3 . (asnjournals.org)
  • We now report that the endogenous peptide, pituitary adenylate cyclase activating polypeptide (PACAP), negatively regulates the cell cycle by inhibiting p57 Kip2 -dependent CDK2 activity in embryonic cortex. (jneurosci.org)
  • Protein levels of CDK2 and members of the CIP/KIP family of CKIs (p27 Kip1 , p57 Kip2 ) were detected in developing rat cortex from embryonic day 13.5 through postnatal day 2. (jneurosci.org)
  • Moreover, decreased kinase activity was accompanied by a twofold increase in levels of p57 Kip2 protein, but not p21 Cip1 or p27 Kip1 , suggesting that p57 Kip2 mediates PACAP anti-mitogenic effects. (jneurosci.org)
  • Indeed, immunoprecipitation of CDK2 complex revealed increased p57 Kip2 association with the kinase and concomitant reduction in free inhibitor after PACAP exposure, suggesting that p57 Kip2 interactions directly regulate CDK2 activity. (jneurosci.org)
  • We have uncovered a novel role for the cyclin-dependent kinase inhibitor, p57 KIP2 , during the immortalization of cultured human mammary epithelial cells (HMECs). (aacrjournals.org)
  • In particular, the CKIs of the Cip/Kip-family (p21 Cip1 , p27 Kip1 , and p57 Kip2 ) have been implicated in bringing about cell-cycle exit during development and in maintaining cells in a terminally differentiated state, demonstrating a cell-selective expression pattern in various organs ( 20 - 25 ). (pnas.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 second cluster is implicated more frequently (approximately 50% of BWS cases) and contains KCNQ1, KCNQ1OT1, and CDKN1C (p57 kip2 ). (renalandurologynews.com)
  • We found that the abundance of the cyclin-dependent kinase inhibitors p21 Cip1 and p57 Kip2 increased in response to IGF-1 or insulin but decreased in response to EGF. (sciencemag.org)
  • Depletion of p57 Kip2 , but not p21 Cip1 , rendered IGF-1 or insulin sufficient to induce cellular proliferation in the absence of EGF. (sciencemag.org)
  • Signaling through the PI3K (phosphatidylinositol 3-kinase)-Akt-mTOR (mammalian target of rapamycin) pathway was necessary and sufficient for the increase in p57 Kip2 , whereas MEK [mitogen-activated or extracellular signal-regulated protein kinase (ERK) kinase]-ERK activity suppressed this increase, forming a regulatory circuit that limited proliferation in response to unaccompanied Akt activity. (sciencemag.org)
  • Knockdown of p57 Kip2 enhanced the proliferative phenotype induced by tumor-associated PI3K mutant variants and released mammary epithelial acini from growth arrest during morphogenesis in three-dimensional culture. (sciencemag.org)
  • These results provide a potential explanation for the context-dependent proliferative activities of insulin and IGF-1 and for the finding that the CDKN1C locus encoding p57 Kip2 is silenced in many breast cancers, which frequently show hyperactivation of the PI3K pathway. (sciencemag.org)
  • The status of p57 Kip2 may thus be an important factor to assess when considering targeted therapy against the ERK or PI3K pathways. (sciencemag.org)
  • This study aims to investigate the expression and significance of p57 kip2 and cyclinD1 in gastric cardia adenocarcinoma (GCA). (oncotarget.com)
  • p57 kip2 is a negative regulator in the cell cycle. (oncotarget.com)
  • Immunohistochemistry and fluorescence qualitative PCR was used to determine the level of p57 kip2 and cyclinD1 in GCA and its adjacent non-cancerous tissues. (oncotarget.com)
  • Furthermore, the correlation between the mRNA/protein and GCA clinical pathologic parameters were analyzed, and the ralationship of p57 kip2 and cyclinD1 in GCA were also evaluated. (oncotarget.com)
  • Furthermore, median survival time was 41 months for patients with high mRNA expression of p57 kip2 . (oncotarget.com)
  • The protein expression of p57 kip2 was not correlated to the protein expression of cyclinD1 ( P = 0.55). (oncotarget.com)
  • Conclusion: The expression of p57 kip2 and cyclinD1 are likely to suppress or promote the tumorigenesis and progression of GCA. (oncotarget.com)
  • In this article we report that stable short hairpin RNA-mediated cortactin knockdown in the 11q13-amplified cell line FaDu led to increased expression of the Cip/Kip cyclin-dependent kinase inhibitors (CDKIs) p21(WAF1/Cip1), p27(Kip1), and p57(Kip2) and inhibition of S-phase entry. (garvan.org.au)
  • The direct roles of p21(WAF1/Cip1), p27(Kip1), and p57(Kip2) downstream of cortactin were confirmed by the transient knockdown of each CDKI by specific small interfering RNAs, which led to partial rescue of cell cycle progression. (garvan.org.au)
  • Interestingly, FaDu cells with reduced cortactin levels also exhibited a significant diminution in RhoA expression and activity, together with decreased expression of Skp2, a critical component of the SCF ubiquitin ligase that targets p27(Kip1) and p57(Kip2) for degradation. (garvan.org.au)
  • The gene of SKP2, located on chromosome 5p13, plays a critical role in cell cycle progression, especially at the G 1 -S transition, putatively through its control of several cell cycle regulator proteins including p27 kip1 , p21 cip1 , p57 kip2 , p130, cyclin E, and c-Myc. (aacrjournals.org)
  • SKP2 has also been implicated in regulating the proteosome-mediated degradation of c-myc, p21 cip1 , p57 kip2 , and p130-Rb2 ( 8 - 13 ). (aacrjournals.org)
  • 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)
  • Here, we evaluate the effects of butyrate (BuA) and other HDACIs on p57 Kip2 , a cyclin-dependent kinase inhibitor (cki). (oup.com)
  • We observed that inhibitors of class I/II histone deacetylases (HDACs), but not of class III HDACs, induce a remarkable accumulation of p57 Kip2 in several cells. (oup.com)
  • The cki upregulation is associated with an increased gene expression that was not prevented by cycloheximide, indicating that HDACIs affect directly p57 Kip2 transcription. (oup.com)
  • The characterization of p57 Kip2 promoter indicates. (oup.com)
  • The characterization of p57 Kip2 promoter indicates that the first 165 bp are mostly involved in the BuA effects. (oup.com)
  • Moreover, both the treatments reduce the p57 Kip2 transcription in untreated cells, suggesting that Sp1 is required for the constitutive cki expression. (oup.com)
  • Studies employing plasmids containing parts of the 165 bp of p57 Kip2 promoter indicate that the promoter region between −87 and −113 bp, which includes two putative Sp1 consensus sequences, plays a critical role in the response to HDACIs. (oup.com)
  • Since this p57 Kip2 promoter region also embraces the consensus sequence for the transcriptional repressor chicken ovalbumin upstream promoter transcription factor-interacting protein 2 (CTIP2), we evaluated whether this factor is involved into the BuA effect. (oup.com)
  • When CTIP2 was downregulated by a specific siRNA, we observed the enhancement of BuA activity on p57 Kip2 expression suggesting that CTIP2 might also be involved in HDACIs effects. (oup.com)
  • Downregulation of CDKN1C (which encodes p57/KIP2 protein) by promoter hypermethylation has been detected with very low frequency in paediatric T-ALL and more often in adult patients. (biomedcentral.com)
  • CDKN1C (p57 kip2 ) encodes a cyclin-dependent kinase inhibitor that negatively regulates cell proliferation, while KCNQ1 encodes part of a potassium channel. (cancertherapyadvisor.com)
  • Recent studies have demonstrated that the use of p57 KIP2 immunostaining improves diagnostic accuracy for CHM. (beds.ac.uk)
  • We will conduct a systematic review of prospective and retrospective studies to evaluate the accuracy of p57 KIP2 immunostaining compared with molecular genotyping for the diagnosis of CHM. (beds.ac.uk)
  • According to our results, p57 KIP2 immunostaining appears to be a practical and accurate adjunct for the diagnosis of CHM and its mimics because this technique is relatively simple, reliable, cost-efficient, and rapid. (beds.ac.uk)
  • This systematic review will help to determine whether p57 KIP2 immunostaining is an adequate alternative diagnostic test for CHM. (beds.ac.uk)
  • The p57 KIP2 gene is paternally imprinted and maternally expressed, and the presence of its protein product serves as a surrogate marker for the nuclear maternal genome. (beds.ac.uk)
  • The index test will consist of p57 KIP2 immunostaining. (beds.ac.uk)
  • P57 KIP2 immunostaining is an in situ technique performed on paraffin-embedded tissue. (beds.ac.uk)
  • The lack of p57 KIP2 activity can lead to a loss of cell cycle control, which results in the abnormal proliferation and differentiation of trophoblasts in CHM. (beds.ac.uk)
  • Transcriptional profile analysis of E14.5 Arx-ablated cortices compared with control revealed that CDKN1C, an inhibitor of cell cycle progression, is overexpressed in the cortical VZ and SVZ of Arx KOs throughout corticogenesis. (nih.gov)
  • CDKN1C , a maternally expressed gene encoding a cyclin-dependent kinase inhibitor, is a negative regulator of fetal growth. (asnjournals.org)
  • To investigate the regulatory effect of microRNA -221 (MIR221) on CDKN1C/p57 expression in colon carcinoma cells in vitro . (bvsalud.org)
  • The MIR221 expression pattern was detected by real- time RT-PCR, and the mRNA and protein levels of CDKN1C/p57 expression were detected using semi-quantitative RT-PCR and Western blotting . (bvsalud.org)
  • CDKN1C/p57 3'-UTR fragment was amplified by PCR from the genome DNA of human colon and inserted into a luciferase reporter plasmid . (bvsalud.org)
  • MIR221 can interact with the target site on the 3'-UTR of CDKN1C/p57 mRNA to inhibit CDKN1C/p57 expression by post-transcriptional gene silencing to promote colon carcinoma cell proliferation , suggesting the value of MIR221 as a potential target for treatment of colon carcinoma . (bvsalud.org)
  • Therefore, levels of cyclins, cyclin-dependent kinases (CDKs), and their regulatory proteins involved in S-G2/M transition were investigated. (hindawi.com)
  • Cell cycle is under sophisticated regulation through the interactions of different cyclins with their specific kinases, cyclin-dependent kinases (CDKs) [ 14 ]. (hindawi.com)
  • Cell cycle progression in eukaryotes is controlled by a series of cyclin-dependent kinases (Cdks) which are in turn modulated by binding to specific cyclins. (asm.org)
  • At the molecular level, production and association of cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors (CKIs) regulate cycle progression. (jneurosci.org)
  • Cycle progression is controlled by pro-mitogenic cyclin-dependent kinases (CDKs) complexed with regulatory cyclins, and anti-mitogenic CDK inhibitors (CKIs). (jneurosci.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)
  • Indeed, the only nuclear G1/S molecules are the cell cycle inhibitors, pRb, p57, and variably, p21: none of the cyclins or cdks necessary to drive human β-cell proliferation are present in the nuclear compartment. (diabetesjournals.org)
  • At the G1 checkpoint, mitogens lead to cyclin D expression which activates cyclin dependent kinases (CDKs) and inactivates Rb. (news-medical.net)
  • Embryonic stem cells have high levels of cyclins A, D and E, meaning that CDKs are constitutively active and Rb is hyper-phosphorylated, so cells bypass the G1 restriction point and can continue to replicate. (news-medical.net)
  • In conclusion, our findings suggested that rMS enhances the NSCs proliferation in vitro in a dose-dependent manner and miR-106b/p21/cdks/cyclins pathway was involved in the process. (bvsalud.org)
  • Cell division in many tissues is regulated by the p27 protein,which binds to and inhibits enzymes called cyclin-dependent kinases(CDKs). (cancernetwork.com)
  • Progression through the different phases of the cell cycle is dependent on the activities of cyclin dependent kinases (cdks) bound to their cognate cyclins [ 1 , 2 ]. (biomedcentral.com)
  • These findings indicate that exposure of 6-gingerol may induce intracellular ROS and upregulate p53, p27 Kip1 , and p21 Cip1 levels leading to consequent decrease of CDK1, cyclin A, and cyclin B1 as result of cell cycle arrest in LoVo cells. (hindawi.com)
  • Here we report that the cyclin-dependent kinase inhibitor p27 Kip1 is selectively expressed in the supporting-cell population of the organ of Corti. (pnas.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)
  • 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)
  • These effects were associated with increased binding of p21(WAF1/Cip1) and p27(Kip1) to cyclin D1- and E1-containing complexes and decreased retinoblastoma protein phosphorylation. (garvan.org.au)
  • Our data are consistent with Shh signalling stimulating polarising region cell proliferation via Cyclin D2, and then inhibiting proliferation via a Bmp2-p27 kip1 pathway. (elifesciences.org)
  • We provide evidence that Shh signalling stimulates the proliferation of polarising region cells via Cyclin D2 and then inhibits proliferation via p27 kip1 . (elifesciences.org)
  • The most important substrates for SKP2 include p27 kip1 cyclin-dependent kinase inhibitor and cyclin E, both of which interact with cyclin-dependent kinase 2 to regulate G 1 -S transition ( 7 ). (aacrjournals.org)
  • We have previously reported changes in protein expression of the cyclin-dependent kinase inhibitors (CDKI), p21CIP1 (CDKN1a), p27KIP1 and p57KIP2 during normal lens cell differentiation and after exposure to Xrays or protons. (arvojournals.org)
  • Seven cyclin-dependent kinase inhibitor proteins have thus far been identified. (wikipedia.org)
  • The discovery of proteins that bind to and inhibit the catalytic activity of cyclin-Cdk complexes has identified kinase inhibition as an intrinsic component of cell cycle control ( 50 ). (asm.org)
  • CDK proteins remain constant throughout the cycle, whereas their activity is modulated by cyclin and CKI association. (jneurosci.org)
  • Immunoprecipitation of CDK4 and CDK6 and their associated proteins from radiolabeled extracts from senescent HDFs showed no other CDK inhibitors. (pnas.org)
  • The researchers' high-tech picture also is likely to have broadimplications for other inhibitory proteins in the p27 family,such as p21 and p57. (cancernetwork.com)
  • Many imprinted genes are involved in growth and development, and as a general rule those that are maternally expressed are growth inhibitors, that those that are paternally expressed are growth promoters. (bioworld.com)
  • The presence of two families of seven distinct mammalian cyclin-dependent kinase (CDK) inhibitor genes is thought to mediate the complexity of connecting a variety of cellular processes to the cell cycle control pathway. (asm.org)
  • The distinct pattern of tissue expression of CDK inhibitor genes suggests that they may function as tumor suppressors with different tissue specificities. (asm.org)
  • Our results suggest that functional collaborations between distinct CDK inhibitor genes are tissue specific and confer yet another level of regulation in cell growth control and tumor suppression. (asm.org)
  • Conceptually, genes that negatively regulate the growth-suppressing activity of either p53 or pRb may be proto-oncogenes, as exemplified by the observation that MDM2 ( 26 ) and cyclin D1 ( 20 ), negative regulators of p53 and pRb, respectively, are frequently activated in human cancers and promote tumor growth when targeted for transgenic expression in mouse mammary tissues ( 22 , 35 ). (asm.org)
  • Two families of cyclin-dependent kinase (CDK) inhibitors, totaling seven genes, have been identified in mammalian cells. (asm.org)
  • Their similar biochemical activity in blocking CDK enzymes and maintaining the growth-suppressive activity of Rb predict a tumor suppression function for CDK inhibitor genes, yet only the p16 INK4a gene has been directly linked to tumor growth by genetic alterations found in human cancers ( 17 , 25 ) and by the early development of spontaneous tumors in mice lacking p16 ( 31 ). (asm.org)
  • Neither mutational analysis in human tumors nor phenotypic examination of genetically targeted mice lacking any of the other individual CDK inhibitor genes has provided strong evidence for a direct role for any of the other CDK inhibitors as tumor suppressors. (asm.org)
  • Rb inactivation leads to expression of E2F-dependent genes such as thymidine kinase, DNA polymerase-α, cdc2, and cyclin A ( 5 ), which are not expressed in senescent cells ( 6 ), indicating that the failure to phosphorylate Rb is important in the growth arrest of senescent cells. (pnas.org)
  • Key target genes in this process include master regulators of the cell cycle, such as cyclin E, which regulates G(1) progression, and cyclin A, which is required for the initiation of DNA synthesis. (semanticscholar.org)
  • First, we found that the IRAK4 kinase activity was required for modified LDL-induced NF-κB activation and expression of a subset of proinflammatory genes but not for the activation of MAPKs in bone marrow-derived macrophage. (jimmunol.org)
  • Various cardiac development related genes involving the cell cycle (cyclin B1, proliferating cell nuclear antigen (PCNA), and Ki67), growth factors (IGF-II, pleiotrophin (PTN), and midkine (MK)), and transcriptional regulation, cytoskeleton, and detoxification enzymes were identified by microarray analysis. (pubmedcentralcanada.ca)
  • 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)
  • During OL differentiation, activity of the G 1 -S phase checkpoint complex CyclinE-cyclin-dependent kinase 2 (cdk2) decreases ( Ghiani and Gallo, 2001 ). (jneurosci.org)
  • G 1 CDK2 and CDK4 kinase activities were increased in both normal and neoplastic tissues derived from mice lacking individual CDK inhibitors and were synergistically stimulated by the simultaneous loss of two CDK inhibitors. (asm.org)
  • Complexes that control mammalian G 1 progression include cyclin E-Cdk2 and Cdk4/Cdk6 associated with any D-type cyclin and become activated upon phosphorylation of the Cdk subunit by CAK (Cdk-activating kinase), itself a Cdk-related kinase complex ( 49 ). (asm.org)
  • CDK2 kinase activity was inhibited 75% by PACAP, whereas kinase protein and its regulatory cyclin E subunit were unaffected. (jneurosci.org)
  • Although early G 1 depends on cyclin D-dependent kinases, the late G 1 /S transition critically depends on cyclin E/CDK2 complexes, which phosphorylate retinoblastoma protein, allowing S-phase gene activation ( Sherr and Roberts, 1999 ). (jneurosci.org)
  • Three cyclin-dependent kinases, CDK2, CDK4, and CDK6, are involved in the phosphorylation of the Rb protein (reviewed in ref. 5 ). (pnas.org)
  • In order to progress through S-phase, CDK2 and CDK1 need to be assembled with cyclin A and cyclin B. (thefreedictionary.com)
  • In general, when the INK group functions in the genetic pathway containing cyclin D-CDK4/6-pRb and E2F, the Cip/Kip group can inhibit CDK2 kinase and CDK4/6 (9), (10). (thefreedictionary.com)
  • The labelling index of skp2 in endometrial carcinoma was significantly correlated with that of p27, Ki-67, cdk2 , cyclin A, cyclin D1, cyclin E, p53 and PTEN. (thefreedictionary.com)
  • CDK2 is activated by cyclin A subunits, and cyclin A is critical for cell cycle control, primarily in the Gl and S phases (Furuno et al. (thefreedictionary.com)
  • These data (Abstract #4972) were presented during a minisymposium on Novel Genomic Approaches, Drugs, Targets, and Strategies in a talk titled "SNS-032, a potent and selective CDK2 , 7 and 9 inhibitor, demonstrates preclinical activity in human multiple myeloma. (thefreedictionary.com)
  • P21 inhibits kinase activity and blocks progression through G1 IS by association with CDK2 complexes (Lo et al. (thefreedictionary.com)
  • SNS-032 Oral Presentation Tuesday, April 15, 2008 -- SNS-032, a potent and selective CDK2 , 7 and 9 inhibitor, demonstrates preclinical activity in human multiple myeloma Minisymposium: Novel Genomic Approaches, Drugs, Targets, and Strategies Abstract #4972 4:55 p. (thefreedictionary.com)
  • The crystal structure reveals that p27 interacts with both membersof the cyclin-kinase complex, in this case cyclin A and CDK2 (see Figure 1 ). (cancernetwork.com)
  • Cyclin-dependent kinase inhibitor 1C is a tight-binding inhibitor of several G1 cyclin/Cdk complexes and a negative regulator of cell proliferation. (wikipedia.org)
  • It encodes a cell cycle inhibitor that binds to G1 cyclin-CDK complexes. (wikipedia.org)
  • Because it is a strong, tight inhibitor of several G1 cyclin/CDK complexes, this protein is a negative regulator of cell proliferation. (cags.org.ae)
  • These cyclin-Cdk complexes can regulate positively the cell cycle by phosphorylating pRB and thereby inhibit the activity of this cell cycle regulator ( 48 , 57 ). (asm.org)
  • They exert these functions by binding to and inactivating cyclin-cyclin-dependent kinase (CDK) complexes. (pnas.org)
  • The team now plans to use x-ray crystallography to reveal howanother class of cell cycle-inhibitors, among them p15 and p16,binds to cyclin-CDK complexes to halt cell division. (cancernetwork.com)
  • Another level of cell cycle regulation is affected by the cdk inhibitors, which bind to cdk or cdk-cyclin complexes and inhibit their kinase activity. (biomedcentral.com)
  • CDK inhibitors: cell cycle regulators and beyond. (springer.com)
  • 11 Several factors including cell cycle regulators (cyclins, cyclin dependent kinases, and proliferating cell nuclear antigen) and oncogenes (c-myc and Rb) are reportedly involved in cardiac muscle cell cycle progression. (pubmedcentralcanada.ca)
  • 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)
  • Cyclins function as regulators of cyclin-dependent kinases. (wikidoc.org)
  • Cell cycle progression is delayed or stopped by cyclin-dependent kinase inhibitors, abbreviated CDIs, CKIs or CDKIs. (wikipedia.org)
  • These Cdk inhibitors (Ckis) induce cell cycle arrest in response to antiproliferative signals, including contact inhibition and serum deprivation ( 42 ), transforming growth factor β ( 44 ), and myogenic ( 41 ), myeloid ( 32 ), and neuronal ( 26 ) differentiation. (asm.org)
  • Inhibitors of cell-cycle progression include the cyclin-dependent kinase inhibitors (CKIs), which function in both cell-cycle arrest and differentiation in other cell types. (pnas.org)
  • As one example, we have only recently learned that loss of the platelet-derived growth factor (PDGF) receptor-α in adult human β-cells, with the resultant loss of ability to activate mitogen-activated protein kinase and methylation (Ezh2) and downstream cell cycle (p16) machinery, may underlie the refractoriness of human β-cells to proliferation ( 16 ). (diabetesjournals.org)
  • Furthermore, there is much evidence for a protective effect of calpain inhibitors, which should inhibit p25 generation. (alzforum.org)
  • This workis important because it establishes a general principle by whichan entire family of inhibitors will block cell growth. (cancernetwork.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)
  • This inhibitor binds to cyclin D, preventing it from entering the nucleus and meaning that CDK4 and CDK6 cannot be activated. (news-medical.net)
  • This cyclin forms a complex with and functions as a regulatory subunit of CDK4 or CDK6 , whose activity is required for cell cycle G1 / S transition. (wikidoc.org)
  • The role of p25 is quite clear and the inhibitor data with the luciferase assay is compelling, but since p25 binds directly to histone deacetylase 1 (HDAC1), do we really need the kinase? (alzforum.org)
  • A cyclin-dependent kinase inhibitor protein is a protein which inhibits the enzyme cyclin-dependent kinase (CDK). (wikipedia.org)
  • Specifically, p27 inhibits cell division by insertingitself into a pocket in the cyclin-CDK complex that normally bindsthe energy molecule adenosine triphosphate (ATP). (cancernetwork.com)
  • This defect is probably not mediated by RSK2-dependent phosphorylation of c-Fos on serine 362 in the C-terminus. (jci.org)
  • This binding can occur in the absence of cyclins and prevents phosphorylation of Rb and thus entry into S-phase. (aacrjournals.org)
  • These data indicate that in HMECs that have overcome replicative senescence, p57 may provide an additional barrier against indefinite proliferation. (aacrjournals.org)
  • One reason for this is that cell number variation between different CNS tissues is also dependent on processes that are distinct from proliferation. (biologists.org)
  • Interestingly, the proliferation markers nuclear transcription factor p63 and cyclin D1 were upregulated, while cyclin-dependent kinase inhibitor p57 was downregulted at both mRNA and protein levels. (arvojournals.org)
  • In addition, the increase in the levels of a G1-S phase inhibitor causes cultured adult oligodendrocyte progenitor cells to differentiate after a defined duration of proliferation ( Durand and Raff, 2000 ). (elifesciences.org)
  • The results showed that rMS could promote NSCs proliferation in a dose-dependent manner. (bvsalud.org)
  • Extracellular-Regulated Protein Kinase 5-Mediated Control of p21 Expression Promotes Macrophage Proliferation Associated with Tumor Growth and Metastasis. (harvard.edu)
  • decrease of p57 leads to increase proliferation and delayed differentiation of chondrocytes. (diff.org)
  • In mammalian cells, two distinct families of CDK inhibitors have been characterized, represented by two prototype CDK inhibitors, p21 and p16. (pnas.org)
  • Three signaling pathways are involved in the UPR, and these are mediated by inositol-requiring enzyme-1 (IRE1, also known as ERN1), PKR-like ER resistant kinase (PERK, also known as EIF2AK3) and activation transcription factor 6 (ATF6), which act in concert to limit new protein synthesis and to increase the levels of chaperones. (biologists.org)
  • The crucial role of DNA-dependent protein kinase and myelin transcription factor 1-like protein in the miR-141 tumor suppressor network. (harvard.edu)
  • PKA then leads to decreases in both p57 levels and in Runx2 mRNA and protein. (diff.org)
  • Here, we review recent advances in cell cycle-dependent cell fate determination and functional heterogeneity, and the application of cell cycle manipulation for cell fate conversion. (springer.com)
  • Our results revealed that 6-gingerol treatment significantly reduced the cell viability of human colon cancer cell, LoVo, in a dose-dependent manner. (hindawi.com)
  • The fully immortal HMECs that grew well did not accumulate p57 in G 0 or during the cell cycle. (aacrjournals.org)
  • At the molecular level terminally differentiated cells have been shown to express high levels of cell-cycle inhibitors, in particular, cyclin-dependent kinase inhibitors [Parker, S. B., et al . (pnas.org)
  • Cyclin D3 promotes pancreatic β-cell fitness and viability in a cell cycle-independent manner and is targeted in autoimmune diabetes. (semanticscholar.org)
  • Deletion of Trp53 rescued the Acvr1 CKO cell death phenotype in embryos and reduced Acvr1 -dependent apoptosis in postnatal lenses. (biologists.org)
  • Deleting Trp53 and Acvr1 showed that most Acvr1 -dependent cell death was mediated by p53. (biologists.org)
  • We now report quantitative gene expression of p21 and p57 during normal lens cell differentiation using our in vitro model system and in a time course after radiation exposure. (arvojournals.org)
  • The aim of this doctoral work was to characterise the nature of cachexia in patients with heart failure (HF) and stable coronary artery disease (CAD), to quantify the loss of muscle mass, and test the hypothesis that muscle wasting is mediated by the activation of tissue cytokines and cell cycle inhibitors. (gla.ac.uk)
  • Skeletal muscle biopsies were analysed for the expression of messenger ribonucleic acid (mRNA) for TNF-α, IL-6, interleukin-1β (IL-1β), interleukin-18 (IL-18) and the cell cycle inhibitors (cyclin dependent kinase (CDK) inhibitors) p21, p27 and p57. (gla.ac.uk)
  • Adult stem cells, however, have cyclin dependent kinase inhibitors (CDKI) and Rb which maintains the restriction point and enable cells to exit the cell cycle. (news-medical.net)
  • Mimics or inhibitors of miR-9 and miR-9(*) were transfected into N2a cells,and the effects of overexpression or knockdown of the microRNAs on the cell cycle were detected by flow cytometry. (bvsalud.org)
  • Cyclin-dependent kinases are so crucial to cell division thatcells--even those that are cancerous--will not multiply withoutthem. (cancernetwork.com)
  • Under normal, healthy conditions, these inhibitors keep cell growthin check as part of a universal pathway that, when altered bygenetic mutations, leads to cancer. (cancernetwork.com)
  • We demonstrated previously that expression of the cell cycle inhibitor p21 is significantly reduced in RA synovial lining, particularly in the FLS. (biomedcentral.com)
  • p21 (-/-) and wild-type (WT) FLS were compared with respect to migration towards chemoattractants found in RA synovial fluid in the presence and absence of cell cycle inhibitors. (biomedcentral.com)
  • As anticipated from the loss of a cell cycle inhibitor, p21 (-/-) FLS grow more rapidly than WT FLS. (biomedcentral.com)
  • Moreover, this effect is independent of the cell cycle since chemical inhibitors that block the cell cycle have no effect on migration. (biomedcentral.com)
  • Overexpression of any of the cdk inhibitors will induce G1-cell cycle arrest [ 3 ]. (biomedcentral.com)
  • A cyclin-dependent kinase inhibitor that mediates TUMOR SUPPRESSOR PROTEIN P53-dependent CELL CYCLE arrest. (harvard.edu)
  • The protein encoded by this gene belongs to the highly conserved cyclin family, whose members are characterized by a dramatic periodicity in protein abundance through the cell cycle . (wikidoc.org)
  • The differentiation was accompanied by a growth arrest and the upregulation of cyclin-dependent kinase inhibitors, p27 and p57, as well as cyclin D 1 , whereas cyclin A was downregulated. (asnjournals.org)
  • Overcoming p57-mediated growth inhibition in these cells may be crucial for acquisition of the unlimited growth potential thought to be critical for malignant progression. (aacrjournals.org)
  • Taken together, our results indicate that the IRAK4 kinase plays an important role in modified LDL-mediated signaling and the development of atherosclerosis, suggesting that pharmacological inhibition of IRAK4 kinase activity might be a feasible approach in the development of antiatherosclerosis drugs. (jimmunol.org)
  • Vikram, we are aware of many studies that show that inhibition of Cdk5 using pharmacological inhibitors or DNK5 can be neuroprotective, for example, in ischemia. (alzforum.org)
  • Collectively, our results highlight the potential roles of ERα and p21 WAF1 in growth inhibition of cancer cells mediated by proteasome inhibitors, such as bortezomib. (aacrjournals.org)
  • In addition, our data indicated that SKP2 promotes anoikis resistance through the phosphoinositidyl 3-kinase (PI3K)-Akt pathway. (aacrjournals.org)
  • p>Describes annotations that are concluded from looking at variations or changes in a gene product such as mutations or abnormal levels and includes techniques such as knockouts, overexpression, anti-sense experiments and use of specific protein inhibitors. (uniprot.org)
  • We also show that the overexpression of p21, p27, and p57 increases the population of Myosin heavy chain (MHC)(+) differentiated cells, thus promoting the cells towards myogenic differentiation. (umn.edu)
  • In transient transfection assays, transcriptional transactivation of the mouse muscle creatine kinase promoter by MyoD was enhanced by the Cdk inhibitors. (asm.org)
  • Regulation of the cyclin D3 promoter by E2F1. (semanticscholar.org)
  • In this study, we aim to investigate the roles of CDKIs such as p21, p27, and p57 in the differentiation process of satellite cells. (umn.edu)
  • Histopathologic features were evaluated along with p57 immunohistochemistry. (bvsalud.org)
  • 3 kb prevented both the slow heterogeneous growth phase and accumulation of p57 in cycling populations. (aacrjournals.org)
  • Complete hydatidiform moles consist only of paternal DNA, and thus the cells lack p57 expression as the gene is paternally imprinted (silenced). (wikipedia.org)
  • DNA and RNA analysis of mass populations and individual subclones of conditionally immortal HMEC line 184A1 showed that continued growth of conditionally immortal cells with critically short telomeres was repeatedly accompanied by loss of the expressed p57 allele and transient expression of the allele imprinted previously. (aacrjournals.org)
  • The p57 gene has been found to be imprinted with preferential expression of the maternal allele (9) , suggesting that loss of the maternal allele by itself may severely reduce p57 expression. (aacrjournals.org)
  • In tumors, methylation was significantly correlated with increased tumor size ( P = 0.0036), lymph node status ( P = 0.0414), tumor stage ( P = 0.0037), cyclin D1 expression ( P = 0.0420), and p16 methylation ( P = 0.0494) and survival ( P = 0.045). (aacrjournals.org)
  • Thus, specific histone deacetylase or methyltransferase inhibitors may provide a means to target GALR1 expression in the most aggressive tumors. (aacrjournals.org)
  • Consistently, deletion of PKD1 promotes expression of the β3-adrenergic receptor (ADRB3) in a CCAAT/enhancerbinding protein (C/EBP)-α and δ-dependent manner, which leads to the elevated expression of beige markers in adipocytes and subcutaneous adipose tissue. (uni-wuerzburg.de)
  • We observed dose-dependent statistically significant radiation-induced changes in the expression of p21 in HLE cells in vitro. (arvojournals.org)
  • Elevated expression of SKP2 protected cancer cells from anoikis, and this effect was mediated, at least in part, by the phosphoinositidyl 3-kinase-Akt pathway. (aacrjournals.org)
  • While the HF-cachexia group had elevated circulating levels of TNF-α and IL-6, there was no increased expression of cytokines or CDK inhibitors in the skeletal muscle. (gla.ac.uk)
  • The presence of Thrombopoietin and TGF-β leads to enhanced p57 expression, which functions as a CDKI. (news-medical.net)
  • In humans, aberrant expression of p57 is associated with various NEOPLASMS as well as with BECKWITH-WIEDEMANN SYNDROME. (bvsalud.org)
  • Different cyclins exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. (wikidoc.org)
  • The publication of a paper describing a mouse model that contained even higher levels of IGF-II, which had more features of Beckwith-Wiedemann syndrome than those mice containing just a double dose of the gene, suggested to Ferguson-Smith that IGF2 may be affecting the animals' phenotype in a dose-dependent manner. (bioworld.com)
  • Anti-p57 has been used as an aide in identification of complete hydatidiform mole (CHM) (no nuclear labeling of cytotrophoblasts and stromal cells) from partial hydatidiform mole (PHM) in which both cytotrophoblasts and stromal cells stain. (biotium.com)
  • Caco2 cells were treated with or without anti-p57- siRNA prior to the addition of pre-MIR221 or anti-MIR221. (bvsalud.org)
  • P57 is a cyclin-dependent kinase inhibitor and tumour suppressor gene located on chromosome 11p15.5. (beds.ac.uk)
  • The figure shows one of the characterized processing patterns of the PTH rP preprohormone, resulting in three bioactive peptides: the N-terminal homologous to PTH, the midregion PTH rP that augments calcium transport and the C-terminal peptide, Osteostatin , that is a potent inhibitor of bone resorption. (diff.org)
  • The cyclin-dependent kinase inhibitors (CDKI) play a major role in this G1/S transition. (umn.edu)
  • 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)
  • Inactivation of the growth factor-regulated S6 kinase RSK2 causes Coffin-Lowry syndrome in humans, an X-linked mental retardation condition associated with progressive skeletal abnormalities. (jci.org)
  • This indicates that an increase in G 1 CDK kinase activity is a critical step during but is not sufficient for tumor growth. (asm.org)
  • 3 kb, infected with retroviruses containing the p57 gene, exhibited premature slow heterogeneous growth. (aacrjournals.org)
  • A small-molecule E2F inhibitor blocks growth in a melanoma culture model. (semanticscholar.org)
  • Treatment of cells with phosphoinositidyl 3-kinase inhibitor (LY294002) and constitutively activator (insulin-like growth factor I) had significant effects on the anoikis of SKP2 RNA interference cells. (aacrjournals.org)
  • As a hormone-dependent disease of continued endometrial growth, endometriosis is predominantly a disease of women of reproductive age. (biomedcentral.com)
  • The invention provides methods for assessing the efficacy of histone deacetylase inhibitors using biomarkers which can be used in human clinical trials and which are more quantitative, easy to be used and more relevant to clinical outcome for PD monitoring than existing assays. (freepatentsonline.com)
  • Histone deacetylase inhibitors (HDACIs) represent a new class of targeted anticancer agents. (oup.com)
  • Protons induce a nearly 5-fold change in p57 in epithelial cells within an hr. after radiation. (arvojournals.org)
  • NeoPalAna: Neoadjuvant Palbociclib, a Cyclin-Dependent Kinase 4/6 Inhibitor, and Anastrozole for Clinical Stage 2 or 3 Estrogen Receptor-Positive Breast Cancer. (semanticscholar.org)