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.
A cyclin subtype that is found associated with CYCLIN-DEPENDENT KINASE 5; cyclin G associated kinase, and PROTEIN PHOSPHATASE 2.
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.
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 B subtype that colocalizes with MICROTUBULES during INTERPHASE and is transported into the CELL NUCLEUS at the end of the G2 PHASE.
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.
A broadly expressed type D cyclin. Experiments using KNOCKOUT MICE suggest a role for cyclin D3 in LYMPHOCYTE development.
A cyclin A subtype primarily found in male GERM CELLS. It may play a role in the passage of SPERMATOCYTES into meiosis I.
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.
A widely-expressed cyclin A subtype that functions during the G1/S and G2/M transitions of the CELL CYCLE.
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.
An unusual cyclin subtype that is found highly expressed in terminally differentiated cells. Unlike conventional cyclins increased expression of cyclin G2 is believed to cause a withdrawal of cells from the CELL CYCLE.
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 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.
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 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 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.
A cyclin subtype that is found associated with CYCLIN-DEPENDENT KINASE 9. Unlike traditional cyclins, which regulate the CELL CYCLE, type T cyclins appear to regulate transcription and are components of positive transcriptional elongation factor B.
A cyclin subtype that is found as a component of a heterotrimeric complex containing cyclin-dependent kinase 7 and CDK-activating kinase assembly factor. The complex plays a role in cellular proliferation by phosphorylating several CYCLIN DEPENDENT KINASES at specific regulatory threonine sites.
The period of the CELL CYCLE preceding DNA REPLICATION in S PHASE. Subphases of G1 include "competence" (to respond to growth factors), G1a (entry into G1), G1b (progression), and G1c (assembly). Progression through the G1 subphases is effected by limiting growth factors, nutrients, or inhibitors.
Cyclin-dependent kinase 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.
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.
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.
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.
A phosphoprotein phosphatase subtype that is comprised of a catalytic subunit and two different regulatory subunits. At least two genes encode isoforms of the protein phosphatase catalytic subunit, while several isoforms of regulatory subunits exist due to the presence of multiple genes and the alternative splicing of their mRNAs. Protein phosphatase 2 acts on a broad variety of cellular proteins and may play a role as a regulator of intracellular signaling processes.
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.
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.
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 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-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 subtype that is found abundantly in post-mitotic tissues. In contrast to the classical cyclins, its level does not fluctuate during the cell cycle.
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.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A cell line derived from cultured tumor cells.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
A continuous cell line of high contact-inhibition established from NIH Swiss mouse embryo cultures. The cells are useful for DNA transfection and transformation studies. (From ATCC [Internet]. Virginia: American Type Culture Collection; c2002 [cited 2002 Sept 26]. Available from http://www.atcc.org/)
Proteins coded by oncogenes. They include proteins resulting from the fusion of an oncogene and another gene (ONCOGENE PROTEINS, FUSION).
The B-cell leukemia/lymphoma-1 genes, associated with various neoplasms when overexpressed. Overexpression results from the t(11;14) translocation, which is characteristic of mantle zone-derived B-cell lymphomas. The human c-bcl-1 gene is located at 11q13 on the long arm of chromosome 11.
A subunit of the interleukin-12 receptor. It plays a role in receptor signaling by associating with JANUS KINASE 2.
An E3 UBIQUITIN LIGASE that interacts with and inhibits TUMOR SUPPRESSOR PROTEIN P53. Its ability to ubiquitinate p53 is regulated by TUMOR SUPPRESSOR PROTEIN P14ARF.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
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 group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
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.
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.
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.
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.
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.
An adenocarcinoma containing finger-like processes of vascular connective tissue covered by neoplastic epithelium, projecting into cysts or the cavity of glands or follicles. It occurs most frequently in the ovary and thyroid gland. (Stedman, 25th ed)
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.
Established cell cultures that have the potential to propagate indefinitely.
A large multisubunit complex that plays an important role in the degradation of most of the cytosolic and nuclear proteins in eukaryotic cells. It contains a 700-kDa catalytic sub-complex and two 700-kDa regulatory sub-complexes. The complex digests ubiquitinated proteins and protein activated via ornithine decarboxylase antizyme.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
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.
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.
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.
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.
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.
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 group of enzymes removing the SERINE- or THREONINE-bound phosphate groups from a wide range of phosphoproteins, including a number of enzymes which have been phosphorylated under the action of a kinase. (Enzyme Nomenclature, 1992)
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.
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.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
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 structurally-diverse family of intracellular-signaling adaptor proteins that selectively tether specific protein kinase A subtypes to distinct subcellular sites. They play a role in focusing the PROTEIN KINASE A activity toward relevant substrates. Over fifty members of this family exist, most of which bind specifically to regulatory subunits of CYCLIC AMP-DEPENDENT PROTEIN KINASE TYPE II such as CAMP PROTEIN KINASE RIIALPHA or CAMP PROTEIN KINASE RIIBETA.
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.
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.
Purifying or cleansing agents, usually salts of long-chain aliphatic bases or acids, that exert cleansing (oil-dissolving) and antimicrobial effects through a surface action that depends on possessing both hydrophilic and hydrophobic properties.
Processes that stimulate the GENETIC TRANSCRIPTION of a gene or set of genes.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
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.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Family of RNA viruses that infects birds and mammals and encodes the enzyme reverse transcriptase. The family contains seven genera: DELTARETROVIRUS; LENTIVIRUS; RETROVIRUSES TYPE B, MAMMALIAN; ALPHARETROVIRUS; GAMMARETROVIRUS; RETROVIRUSES TYPE D; and SPUMAVIRUS. A key feature of retrovirus biology is the synthesis of a DNA copy of the genome which is integrated into cellular DNA. After integration it is sometimes not expressed but maintained in a latent state (PROVIRUSES).
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.

Cyclin G2 associates with protein phosphatase 2A catalytic and regulatory B' subunits in active complexes and induces nuclear aberrations and a G1/S phase cell cycle arrest. (1/25)

Cyclin G2, together with cyclin G1 and cyclin I, defines a novel cyclin family expressed in terminally differentiated tissues including brain and muscle. Cyclin G2 expression is up-regulated as cells undergo cell cycle arrest or apoptosis in response to inhibitory stimuli independent of p53 (Horne, M., Donaldson, K., Goolsby, G., Tran, D., Mulheisen, M., Hell, J. and Wahl, A. (1997) J. Biol. Chem. 272, 12650-12661). We tested the hypothesis that cyclin G2 may be a negative regulator of cell cycle progression and found that ectopic expression of cyclin G2 induces the formation of aberrant nuclei and cell cycle arrest in HEK293 and Chinese hamster ovary cells. Cyclin G2 is primarily partitioned to a detergent-resistant compartment, suggesting an association with cytoskeletal elements. We determined that cyclin G2 and its homolog cyclin G1 directly interact with the catalytic subunit of protein phosphatase 2A (PP2A). An okadaic acid-sensitive (<2 nm) phosphatase activity coprecipitates with endogenous and ectopic cyclin G2. We found that cyclin G2 also associates with various PP2A B' regulatory subunits, as previously shown for cyclin G1. The PP2A/A subunit is not detectable in cyclin G2-PP2A-B'-C complexes. Notably, cyclin G2 colocalizes with both PP2A/C and B' subunits in detergent-resistant cellular compartments, suggesting that these complexes form in living cells. The ability of cyclin G2 to inhibit cell cycle progression correlates with its ability to bind PP2A/B' and C subunits. Together, our findings suggest that cyclin G2-PP2A complexes inhibit cell cycle progression.  (+info)

Control of cyclin G2 mRNA expression by forkhead transcription factors: novel mechanism for cell cycle control by phosphoinositide 3-kinase and forkhead. (2/25)

Cyclin G2 is an unconventional cyclin highly expressed in postmitotic cells. Unlike classical cyclins that promote cell cycle progression, cyclin G2 blocks cell cycle entry. Here we studied the mechanisms that regulate cyclin G2 mRNA expression during the cell cycle. Analysis of synchronized NIH 3T3 cell cultures showed elevated cyclin G2 mRNA expression levels at G(0), with a considerable reduction as cells enter cell cycle. Downregulation of cyclin G2 mRNA levels requires activation of phosphoinositide 3-kinase, suggesting that this enzyme controls cyclin G2 mRNA expression. Because the phosphoinositide 3-kinase pathway inhibits the FoxO family of forkhead transcription factors, we examined the involvement of these factors in the regulation of cyclin G2 expression. We show that active forms of the forkhead transcription factor FoxO3a (FKHRL1) increase cyclin G2 mRNA levels. Cyclin G2 has forkhead consensus motifs in its promoter, which are transactivated by constitutive active FoxO3a forms. Finally, interference with forkhead-mediated transcription by overexpression of an inactive form decreases cyclin G2 mRNA expression levels. These results show that FoxO genes regulate cyclin G2 expression, illustrating a new role for phosphoinositide 3-kinase and FoxO transcription factors in the control of cell cycle entry.  (+info)

Effect of cyclin G2 on proliferative ability of SGC-7901 cell. (3/25)

AIM: To study the effect of cyclin G2 on proliferation of gastric adenocarcinoma cell line-SGC-7901 cell in vitro. METHODS: By use of cation lipofectamine transfection reagent, the pIRES-G2 and pIRESneo plasmids were transferred into SGC-7901cell line. Anticlones were selected by G418. Positive clones were observed and counted using Giemsa staining. Cell proliferative ability was assayed by MTT. RESULTS: (1) The clone number of pIRES-G2 group decreased, clone volume reduced. The number of cell clones in pIRESneo group was 87+/-3, that of pIRES-G2 group was 53+/-4, occupying 60.1% of pIRESneo group, there was significant difference obviously (P<0.01, t=15.45). (2) The average absorbance of clone cell obtained by stable transfection of pIRES-G2 at 570 nm was 1.6966+/-0.2125, the average absorbance of clone cell obtained by stable transfection of pIRESneo at 570 nm was 2.1182+/-0.3675, there was significant difference between them (P<0.01, t=3.412). CONCLUSION: Cyclin G2 can inhibit SGC-7901cell proliferative ability obviously, it may be a negative regulator in cell cycle regulation.  (+info)

Cyclin G2 dysregulation in human oral cancer. (4/25)

Using expression microarray, we have previously shown that human cyclin G2 (hCG2) is significantly down-regulated in laser capture microdissected oral cancer epithelia. Western analysis showed detectable hCG2 protein in normal (2 of 2) but not in malignant (4 of 4) oral keratinocyte cell lines. Immunohistochemistry analysis done on oral cancers showed that normal oral mucosa (100%, 12 of 12) and 69.1% (47 of 68) of dysplastic oral epithelia expressed readily detectable hCG2 in the nuclei. However, only 11.1% of oral cancer epithelia (14 of 126) showed mild hCG2 nuclear staining. Interestingly, of the oral cancers devoid of nuclear hCG2 (112 cases), 58 cases (52%) showed cytoplasmic hCG2 immunostaining, whereas the other 54 cases (48%) exhibited neither nuclear nor cytoplasmic hCG2 staining. In vitro functional study by ectopic restoration of hCG2 expression in the human malignant squamous cell carcinoma (SCC) line SCC15 resulted in a significant inhibition of cellular proliferation (P < 0.001) and colony formation (P < 2 x 10(-5)) with increased population of G(1) phase and decreased in S phase (P < 0.01). Furthermore, stable down-regulation of hCG2 by short interference RNA-based gene silencing in immortalized normal oral keratinocytes resulted in enhanced cell growth with increase in S and prominently in G(2) phase. Because hCG2 has been implicated as a negative regulator in cell cycle progression, our results support that hCG2 dysregulation may play an important role in epithelial transformation and the early stages of human oral cancer development.  (+info)

Cellular and gene expression responses involved in the rapid growth inhibition of human cancer cells by RNA interference-mediated depletion of telomerase RNA. (5/25)

Inhibition of the up-regulated telomerase activity in cancer cells has previously been shown to slow cell growth but only after prior telomere shortening. Previously, we have reported that, unexpectedly, a hairpin short interfering RNA specifically targeting human telomerase RNA rapidly inhibits the growth of human cancer cells independently of p53 or telomere length and without bulk telomere shortening (Li, S., Rosenberg, J. E., Donjacour, A. A., Botchkina, I. L., Hom, Y. K., Cunha, G. R., and Blackburn, E. H. (2004) Cancer Res. 64, 4833-4840). Here we have demonstrated that such telomerase RNA knockdown in cancer cells does not cause telomere uncapping but rather induces changes in the global gene expression profile indicative of a novel response pathway, which includes suppression of specific genes implicated in angiogenesis and metastasis, and is distinct from the expression profile changes induced by telomere-uncapping mutant template telomerase RNAs. These cellular responses to depleting telomerase in human cancer cells together suggest that cancer cells are "telomerase-addicted" and uncover functions of telomerase in tumor growth and progression in addition to telomere maintenance.  (+info)

FOXO transcription factors cooperate with delta EF1 to activate growth suppressive genes in B lymphocytes. (6/25)

Forkhead transcription factors regulate many aspects of lymphocyte development and function. The FOXO subgroup of Forkhead factors opposes proliferation and survival, and FOXO inactivation is an important outcome of Ag receptor signaling. FOXO activity at target promoters is modulated by other transcription factors in a manner dependent on cell type and external stimulus. We have investigated the mechanisms by which FOXO proteins activate the promoters of two target genes in murine B lymphocytes, Ccng2 (encoding cyclin G2) and Rbl2 (p130), each of which has been implicated in cell cycle arrest. FOXO proteins bound directly to both promoters in vitro and in vivo, augmented transcriptional activity in reporter assays, and increased expression of the endogenous genes. Each of the promoter sequences has consensus binding sites for the deltaEF1 transcription factor, previously shown to either repress or activate different promoters. deltaEF1 bound to the Ccng2 and Rbl2 promoters in vitro and in vivo and increased reporter activity as well as endogenous mRNA levels for these genes. Strikingly, deltaEF1 synergized with FOXO proteins to strongly activate transcription from both promoters. Coexpression of deltaEF1 enhanced FOXO-induced cell cycle arrest in B lymphoma cells. These findings establish a novel mechanism of FOXO function at target promoters: cooperation with deltaEF1.  (+info)

Estrogen-occupied estrogen receptor represses cyclin G2 gene expression and recruits a repressor complex at the cyclin G2 promoter. (7/25)

Estrogens, acting through their nuclear receptors have a broad impact on target cells, eliciting a transcriptional response program that involves gene repression as well as gene stimulation. While much is known about the mechanisms by which the estrogen-occupied estrogen receptor (ER) stimulates gene expression, the molecular events that lead to gene repression by the hormone-ER complex are largely unknown. Because estradiol represses expression of the cyclin G2 gene, which encodes a negative regulator of the cell cycle, our aim was to understand the mechanism by which cyclin G2 is repressed by estrogen. We show that cyclin G2 is a primary ER target gene in MCF-7 breast cancer cells that is rapidly and robustly down-regulated by estrogen. Promoter analysis reveals a responsive region containing a half-estrogen response element and GC-rich region that interact with ER and Sp1 proteins. Mutation of the half-ERE abrogates hormone-mediated repression. Mutational mapping of receptor reveals a requirement for its N-terminal region and DNA binding domain to support cyclin G2 repression. Following estradiol treatment of cells, chromatin immunoprecipitation analyses reveal recruitment of ER to the cyclin G2 regulatory region, dismissal of RNA polymerase II, and recruitment of a complex containing N-CoR and histone deacetylases, leading to a hypoacetylated chromatin state. Our study provides evidence for a mechanism by which the estrogen-occupied ER is able to actively repress gene expression in vivo and indicates a role for nuclear receptor corepressors and associated histone deacetylase activity in mediating negative gene regulation by this hormone-occupied nuclear receptor.  (+info)

Cyclin G2 is a centrosome-associated nucleocytoplasmic shuttling protein that influences microtubule stability and induces a p53-dependent cell cycle arrest. (8/25)

Cyclin G2 is an atypical cyclin that associates with active protein phosphatase 2A. Cyclin G2 gene expression correlates with cell cycle inhibition; it is significantly upregulated in response to DNA damage and diverse growth inhibitory stimuli, but repressed by mitogenic signals. Ectopic expression of cyclin G2 promotes cell cycle arrest, cyclin dependent kinase 2 inhibition and the formation of aberrant nuclei [Bennin, D. A., Don, A. S., Brake, T., McKenzie, J. L., Rosenbaum, H., Ortiz, L., DePaoli-Roach, A. A., and Horne, M. C. (2002). Cyclin G2 associates with protein phosphatase 2A catalytic and regulatory B' subunits in active complexes and induces nuclear aberrations and a G(1)/S-phase cell cycle arrest. J Biol Chem 277, 27449-67]. Here we report that endogenous cyclin G2 copurifies with centrosomes and microtubules (MT) and that ectopic G2 expression alters microtubule stability. We find exogenous and endogenous cyclin G2 present at microtubule organizing centers (MTOCs) where it colocalizes with centrosomal markers in a variety of cell lines. We previously reported that cyclin G2 forms complexes with active protein phosphatase 2A (PP2A) and colocalizes with PP2A in a detergent-resistant compartment. We now show that cyclin G2 and PP2A colocalize at MTOCs in transfected cells and that the endogenous proteins copurify with isolated centrosomes. Displacement of the endogenous centrosomal scaffolding protein AKAP450 that anchors PP2A at the centrosome resulted in the depletion of centrosomal cyclin G2. We find that ectopic expression of cyclin G2 induces microtubule bundling and resistance to depolymerization, inhibition of polymer regrowth from MTOCs and a p53-dependent cell cycle arrest. Furthermore, we determined that a 100 amino acid carboxy-terminal region of cyclin G2 is sufficient to both direct GFP localization to centrosomes and induce cell cycle inhibition. Colocalization of endogenous cyclin G2 with only one of two GFP-centrin-tagged centrioles, the mature centriole present at microtubule foci, indicates that cyclin G2 resides primarily on the mother centriole. Copurification of cyclin G2 and PP2A subunits with microtubules and centrosomes, together with the effects of ectopic cyclin G2 on cell cycle progression, nuclear morphology and microtubule growth and stability, suggests that cyclin G2 may modulate the cell cycle and cellular division processes through modulation of PP2A and centrosomal associated activities.  (+info)

CCNG2 gene was initially identified in 1996 and encodes for a protein that belongs to a family of cyclins homologous to CCNG1 (7). Previous studies have reported that CCNG2 participates in carcinogenesis and is a known tumor suppressor gene (15-17,20-26). CCNG2 gene expression is downregulated in thyroid (20), oral (21), ovarian (22), breast (23,24), gastric (16), esophageal (17), prostate (25), kidney (26) and colorectal (15) cancer cells.. Several aspects of CCNG2 behavior are associated with antitumor effects. Antitumor agents induce CCNG2 expression, which results in the inhibition of cancer cell proliferation (8-10). In breast cancer, CCNG2 knockdown induces multidrug resistance (8). In colorectal cancer, CCNG2 expression correlates with the tumor stage, lymph node metastasis, clinical stage, histological grade and overall survival (15). In gastric cancer, CCNG2 expression correlates with the extent of differentiation: CCNG2 expression is high in well-differentiated adenocarcinomas and low ...
Rabbit monoclonal antibody raised against a human CCNG1 peptide using ARM Technology. A synthetic peptide of human CCNG1 is used for rabbit immunization.Customer or Abnova will decide on the preferred peptide sequence. (H00000900-K) - Products - Abnova
79 ccng2 TaqMan 5-nuclease assay chemistry provides a fast and simple way to get single nucleotide polymorphism (SNP) genotyping results.
Transcriptional regulator which directly modulates PDPK1 expression, thus promoting survival of pancreatic beta-cells. Also regulates expression of NDFIP1, BNIP3, and CCNG1.
An Integrated Bioinformatics Approach Identifies Elevated Cyclin E2 Expression and E2F Activity as Distinct Features of Tamoxifen Resistant Breast Tumors. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
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Hepatitis B virus (HBV) X protein (HBx) reported to be associated with pathogenesis of hepatocellular carcinoma (HCC) and miR-122 expression is down regulated in HCC. Previous studies reported miR-122 targets cyclin G1 (CCNG1) expression and this in turn abolishes p53-mediated inhibition of HBV replication. Here we investigated the involvement of HBx protein in the modulation of miR-122 expression in hepatoblastoma cells. Expression of miR-122 was measured in HepG2 cells transfected with HBx plasmid (HBx-HepG2), full length HBV genome (HBV-HepG2) and in constitutively HBV synthesizing HepG2.2.15 cells. CCNG1 mRNA (a direct target of miR-122) and protein expressions were also measured in both HBx-HepG2, HBV-HepG2 cells and in HepG2.2.15 cells. miR-122 expressions were analyzed in HBx-HepG2, HBV-HepG2 and in HepG2.2.15 cells after treatment with HBx mRNA specific siRNA. Expressions of p53 mRNA and protein which is negatively regulated by CCNG1 were analyzed in HBx transfected HepG2 cells; X silenced HBx
Complete information for CNOT4 gene (Protein Coding), CCR4-NOT Transcription Complex Subunit 4, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Complete information for CNOT6 gene (Protein Coding), CCR4-NOT Transcription Complex Subunit 6, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
CNOT4 - CNOT4 (Myc-DDK-tagged)-Human CCR4-NOT transcription complex, subunit 4 (CNOT4), transcript variant 1 available for purchase from OriGene - Your Gene Company.
CNOT4 - CNOT4 (Myc-DDK-tagged)-Human CCR4-NOT transcription complex, subunit 4 (CNOT4), transcript variant 3 available for purchase from OriGene - Your Gene Company.
Stack Exchange network consists of 176 Q&A communities including Stack Overflow, the largest, most trusted online community for developers to learn, share their knowledge, and build their careers. Visit Stack Exchange ...
Objective: Light blood cell (WBC) count to mean platelet volume (MPV) percentage (WMR) is associated with major adverse cardiovascular events in patients with non-ST elevation acute coronary syndrome (NSTEMI). the tertiles. Results: WMR was significantly higher in the CCNG2 patient group compared to the control group (p 0,001). WMR among low, intermediate and high score tertiles were determined to be 89026, 1090042 and 150065, respectively (p 0,001). In receiver operating characteristics (ROC) analysis, WMR 960 3-Hydroxydodecanoic acid expected a SYNTAX score 23 with 80.6% level of sensitivity and 67.6% specificity (AUC: 0.756; 95% CI: 0.685 - 0.818; p 0.0001) and a WMR 1360 predicted a SYNTAX score 33 with 71.4% level of sensitivity and 93% specificity (AUC: 0.840; 95%CI: 0.777 - 0.892; p 0.0001). Conclusions: WMR value was significantly elevated in NSTEMI individuals, compared to settings. Higher WMR was associated with higher SYNTAX score in individuals with NSTEMI. WMR 3-Hydroxydodecanoic ...
In the late G2 phase, it is present as an inactive complex of tyrosine-phosphorylated p34cdc2 and unphosphorylated cyclin ... As cells leave the S phase and enter the G2 phase, a massive tyrosine phosphorylation of p34cdc2 occurs. Regulation with ... Meijer L, Azzi L, Wang JY (1991). "Cyclin B targets p34cdc2 for tyrosine phosphorylation". EMBO J. 10 (6): 1545-54. doi:10.1002 ...
The Cdc25 enzymes Cdc25A-C are known to control the transitions from G1 to S phase and G2 to M phase. The structure of Cdc25 ... Cdc25 activates cyclin dependent kinases by removing phosphate from residues in the Cdk active site. In turn, the ... Cyclin "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine. cdc25+ ... May 1991). "Dephosphorylation and activation of a p34cdc2/cyclin B complex in vitro by human CDC25 protein". Nature. 351 (6323 ...
In the context of endoreplication these events are facilitated by an oscillation in cyclin E-Cdk2 activity. Cyclin E-Cdk2 ... Endoreplication can be understood simply as a variant form of the mitotic cell cycle (G1-S-G2-M) in which mitosis is ... de Nooij JC; Graber KH; Hariharan IK (2001). "Expression of cyclin-dependent kinase inhibitor Dacapo is regulated by cyclin E ... Post-transcriptional regulation of cyclin E-Cdk2 activity involves Ago/Fbw7-mediated proteolytic degradation of cyclin E and ...
All these phases in the cell cycle are highly regulated by cyclins, cyclin-dependent kinases, and other cell cycle proteins. ... The first process, non-homologous end joining (NHEJ), can join the two broken ends of DNA in the G1, S and G2 phases of ... Thus, a cell grows (G1), continues to grow as it duplicates its chromosomes (S), grows more and prepares for mitosis (G2), and ... HRR is active during the S and G2 phases of interphase when DNA replication is either partially accomplished or after it is ...
... and G2 phases and passed all the necessary checkpoints. Many factors including cyclins, cyclin-dependent kinases (CDKs), ... APC ubiquitinates nine-amino acid motif known as the destruction box (D box) in the NH2-terminal domain of mitotic cyclins for ... Cdc20 and Cdh1, which are the activators of APC, recruit substrates such as securin and B-type cyclins(Clb) for ubiquitination ... Cdk1-inhibitors could induce mitotic exit even when degradation of B-type cyclins was blocked by expression of non-degradable ...
This gene targets the cyclin-dependent kinase inhibitor, p21, and causes cell differentiation, cell cycle arrest in G1, and ... which result in the K562 cells being arrested in the G2/M phase of the cell cycle. This arrest leads to "shrinkage, blebbing, ...
The gene is also mapped to 6 G2-G3 on the mouse chromosome, and 4q43 distal-q4 on the rat chromosome respectively.[13] BHLHE41 ... Breast cancer tumors that show high expression of BHLHE41 and CyclinG2 are believed to have a lower metastatic risk.[37][38] ...
Well-characterized cell cycle substrates of SCF complexes include: cyclin family proteins: Cyclin D, Cyclin E transcriptional ... The anaphase-promoting complex (APC) controls the metaphase-anaphase transition, while the SCF complex controls G1/S and G2/M ... SCF-fbxo4 plays a role in cell cycle control by targeting cyclin D1 for degradation. Cyclin F is an FBP that is associated with ... Mutations that prevent phosphorylation of Cyclin F alter the activity of SCF-Cyclin F, which likely affects downstream ...
Entry into M phase is controlled through the activation of cyclin-dependent kinase 1 (CDK1)-cyclin B, and Cdc25 is a ... Plk has also been shown to be needed at the G2/M transition. Spindle pole formation needs Plk1, and some proteins such as gamma ...
Wee1 acts to keep Cdc2 inactive during early G2 when cells are still small. When cells have reached sufficient size during G2, ... These transitions are controlled by the cyclin-dependent kinase Cdk1.[10] Though the proteins that control Cdk1 are well ... It is not until the cells grow into late G2, when Pom1 is confined to the cell ends that Cdr2 in the medial cortical nodes is ... A cell is unable to get too small because the later cell cycle events, such as S, G2, and M, are delayed until mass increases ...
cyclin binding. • cyclin-dependent protein kinase activating kinase activity. • cyclin-dependent protein serine/threonine ... G2/M transition of mitotic cell cycle. • positive regulation of B cell proliferation. • negative regulation of cell growth. • ... p21Cip1 (alternatively p21Waf1), also known as cyclin-dependent kinase inhibitor 1 or CDK-interacting protein 1, is a cyclin- ... CDKN1A, CAP20, CDKN1, CIP1, MDA-6, P21, SDI1, WAF1, p21CIP1, cyclin-dependent kinase inhibitor 1A, cyclin dependent kinase ...
... including several cyclin and cyclin-dependent kinase molecules as they correspond to the S, M, G1 and G2 phases of the cell ... partially corresponding to G1 and G2) in which mass, via a stable point, controls cyclin levels, and phases (S and M phases) in ... Tech and Institut de Génétique et Développement de Rennes produced a simplified model of the cell cycle using only one cyclin/ ...
G2/M cyclins - essential for the control of the cell cycle at the G2/M transition (mitosis). G2/M cyclins accumulate steadily ... 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 ... cyclin D (Cdk4) cyclin E (Cdk2) cyclin E, A (Cdk2,1) cyclin A, B, B3 (Cdk1) ...
Regulation of cyclin A-Cdk2 by SCF component Skp1 and F-box protein Skp2. „Mol. Cell. Biol.". 19 (1), s. 635-45, 1999. PMID: ... Identification of a functional domain in a GADD45-mediated G2/M checkpoint. „J. Biol. Chem.". 275 (47), s. 36892-8, 2000. DOI: ... Li Y, Jenkins CW, Nichols MA, Xiong Y. Cell cycle expression and p53 regulation of the cyclin-dependent kinase inhibitor p21. „ ... Watanabe H, Pan ZQ, Schreiber-Agus N, DePinho RA, Hurwitz J, Xiong Y. Suppression of cell transformation by the cyclin- ...
positive regulation of G2/M transition of mitotic cell cycle. • response to toxic substance. • positive regulation of cell ... cyclin-dependent protein serine/threonine kinase regulator activity. • protein binding. • ATP binding. • cyclin binding. • ... Component of the ternary complex, cyclin D/CDK4/CDKN1B, required for nuclear translocation and activity of the cyclin D-CDK4 ... 1993). "Direct binding of cyclin D to the retinoblastoma gene product (pRb) and pRb phosphorylation by the cyclin D-dependent ...
Cells undergoing cell division exhibit hysteresis in that it takes a higher concentration of cyclins to switch them from G2 ...
regulation of cyclin-dependent protein serine/threonine kinase activity. • G1/S transition of mitotic cell cycle. • G2/M ... cyclin-dependent protein kinase activating kinase activity. • cyclin binding. • ubiquitin protein ligase binding. • protein ... cyclin-dependent protein kinase holoenzyme complex. • nucleus. • nucleoplasm. • cytosol. • intracellular membrane-bounded ... Cyclin-dependent kinase inhibitor 1A (p21, Cip1). Structure of the C-terminal region of p21(WAF1/CIP1) complexed with human ...
제2간기인 G2 단계가 지나 전기가 되면 방추체와 미세소관이 형성되고 유전체는 염색질을 이루어 뭉치게 된다. 염색질은 DNA가 여러 차례 꼬여져 만들어진 보다 굵고 단단한 실과 같은 형태이다. 염색질은 다시 염색체를 형성하게 ... 사이클린이 특정 농도 이상이 되면 사이클린 의존성 키나아제(Cyclin-dependent Kinase, Cdk)와 결합하여 사이클린-Cdk 복합체를 만든다. Cdk는 여러 종류가 있으며 각각 Cdk-1, Cdk-2 와 같은 ... 간기를 세분하면 평상적인 생장과 대사를 하는 제1간기(G1), 유전체를 복제하여 세포 분열을 준비하는 합성기(S), 미세소관을 만드는 데 필요한 단백질을 형성하는 제2간기(G2)의 세 기긴으로 다시 나뉠 수 있다.[27] ...
The cell cycle is divided into four distinct phases, G1, S, G2, and M. The G phases - which is the cell growth phase - makes up ... The cell cycle is regulated by a series of signalling factors and complexes such as cyclin-dependent kinases and p53, to name a ...
HIV-1 expression induces tubular cell G2/M arrest and apoptosis.[94] The progression from HIV to AIDS is not immediate or even ... Cyclin. *A (A1, A2). *B (B1, B2, B3). *D (D1, D2, D3) ... "HIV-1 Expression Induces Tubular Cell G2/M Arrest and ...
Rakutsükkel M-mitoosifaas;raku jagunemine, G0-puhkefaas;rakk ei jagune, G1-valmistumine DNA sünteesiks,S-replikatsioonifaas, G2 ... Intracellular Control of Cell-Cycle Events: S-Phase Cyclin-Cdk Complexes (S-Cdks) Initiate DNA Replication Once Per Cycle. ...
SLBP are marked for degradation by phosphorylation at two threonine residues by cyclin dependent kinases, possibly cyclin A/ ... for example in pericentric heterochromatin of cells during G2. H3S10 phosphorylation has also been linked to DNA damage caused ... NPAT activates histone gene expression only after it has been phosphorylated by the G1/S-Cdk cyclin E-Cdk2 in early S phase.[ ... NPAT is also a substrate of cyclin E-Cdk2, which is required for the transition between G1 phase and S phase. ...
cyclin-dependent protein kinase inhibitor activity. • protein binding. • transcription factor binding. • protein kinase binding ... regulation of G2/M transition of mitotic cell cycle. • negative regulation of cell growth. • negative regulation of B cell ... negative regulation of cyclin-dependent protein kinase activity. • negative regulation of transcription, DNA-dependent. • ...
Arif A, Jia J, Moodt RA, DiCorleto PE, Fox PL (January 2011). "Phosphorylation of glutamyl-prolyl tRNA synthetase by cyclin- ...
cyclin binding. • cyclin-dependent protein kinase activating kinase activity. • cyclin-dependent protein serine/threonine ... G2/M transition of mitotic cell cycle. • positive regulation of B cell proliferation. • negative regulation of cell growth. • ... CDKN1A, CAP20, CDKN1, CIP1, MDA-6, P21, SDI1, WAF1, p21CIP1, cyclin-dependent kinase inhibitor 1A, cyclin dependent kinase ... cyclin-dependent protein kinase holoenzyme complex. • PCNA-p21 complex. • perinuclear region of cytoplasm. • клітинне ядро. • ...
... cyclins and cyclin dependent kinases". Oncogene. 15 (2): 143-57. doi:10.1038/sj.onc.1201252. PMID 9244350.. ... mitotic G2/M transition checkpoint. • regulation of transcription from RNA polymerase II promoter. • negative regulation of G0 ... signal transduction involved in G2 DNA damage checkpoint. • regulation of signal transduction by p53 class mediator. ... "BRCA1 phosphorylation by Aurora-A in the regulation of G2 to M transition". J. Biol. Chem. 279 (19): 19643-8. doi:10.1074/jbc. ...
G2. pośrednio zróżnicowany nowotwór - niski stopień złośliwości histologicznej. G3. źle zróżnicowany nowotwór - wysoki stopień ... The cyclin-dependent kinase inhibitor SCH 727965 (dinacliclib) induces the apoptosis of osteosarcoma cells. „Mol Cancer Ther". ...
"CDK-dependent Hsp70 Phosphorylation controls G1 cyclin abundance and cell-cycle progression". Cell. 151 (6): 1308-18. doi ...
... cyclins and cyclin dependent kinases». Oncogene. 15 (2): 143-57. PMID 9244350. doi:10.1038/sj.onc.1201252. !CS1 manut: Nomes ... Durante a fase S/G2 do ciclo celular BRCA1 é liberado formando o complexo BRCA1-CtIP-MRN, que retira 53BP1 da região de quebra ... cyclins and cyclin dependent kinases». Oncogene. 15 (2): 143-57. PMID 9244350. doi:10.1038/sj.onc.1201252. A referência emprega ... mitotic G2/M transition checkpoint. • regulation of transcription from RNA polymerase II promoter. • negative regulation of G0 ...
G2/M transition of mitotic cell cycle. • regulation of actin polymerization or depolymerization. • Golgi organization. • ... Liu H, Di Cunto F, Imarisio S, Reid LM (Jan 2003). "Citron kinase is a cell cycle-dependent, nuclear protein required for G2/M ...
Rakutsükkel M-mitoosifaas;raku jagunemine, G0-puhkefaas;rakk ei jagune, G1-valmistumine DNA sünteesiks,S-replikatsioonifaas, G2 ... Intracellular Control of Cell-Cycle Events: S-Phase Cyclin-Cdk Complexes (S-Cdks) Initiate DNA Replication Once Per Cycle. ...
Wee1 acts to keep Cdc2 inactive during early G2 when cells are still small. When cells have reached sufficient size during G2, ... These transitions are controlled by the cyclin-dependent kinase Cdk1.[6] Though the proteins that control Cdk1 are well ... It is not until the cells grow into late G2, when Pom1 is confined to the cell ends that Cdr2 in the medial cortical nodes is ... A cell is unable to get too small because the later cell cycle events, such as S, G2, and M, are delayed until mass increases ...
Zhao L, Samuels T, Winckler S, Korgaonkar C, Tompkins V, Horne MC, Quelle DE (January 2003). "Cyclin G1 has growth inhibitory ... "The MDM2 C-terminal region binds to TAFII250 and is required for MDM2 regulation of the cyclin A promoter". The Journal of ...
Nguyen VQ, Co C, Li JJ (June 2001). "Cyclin-dependent kinases prevent DNA re-replication through multiple mechanisms". Nature ... incluíndo o bloqueo da reiniciación na fase G2/fase M.[5][15][16][17] ... "Binding of cyclin-dependent kinases to ORC and Cdc6p regulates the chromosome replication cycle". Proc. Natl. Acad. Sci. U.S.A ...
Cyclin G2 (CCNG2; encoded by CCNG2 gene) belongs to a family of cyclins homologous to CCNG1 (7). Cyclins positively regulate ... Choi MG, Noh JH, An JY, Hong SK, Park SB, Baik YH, Kim KM, Sohn TS and Kim S: Expression levels of cyclin G2, but not cyclin E ... Unlike other cyclins that positively regulate the cell cycle, cyclin G2 (CCNG2) regulates cell proliferation as a tumor ... i] CCNG2, cyclin G2; NS, not significant; Ph/Pb/Pt, pancreatic head/body/tail; (+/-), yes/no; well/mod/poor, well/moderately/ ...
The nucleotide sequence of cyclin G1 and cyclin G2 are 53% identical. Unlike cyclin G1, cyclin G2 contains a C-terminal PEST ... cyclin G2. -. -. rs4150052. C__25994756_10 details, C__25994756_10 search Human. cyclin G2. -. XM_011532398.1;NM_004354.2;XM_ ... cyclin G2. -. -. -. C__32298847_10 details, C__32298847_10 search Human. cyclin G2. -. XM_011532398.1;NM_004354.2;XM_ ... cyclin G2. -. XM_011532398.1;NM_004354.2;XM_011532399.2. rs2306410. C__61628197_10 details, C__61628197_10 search Human. cyclin ...
We interviewed CNS "graduate" Ray Ydoyaga about his personal experiences at BORP. Ray started out riding recumbent cycles with the CNS group, has become a regular independent rider, and just this month successfully got back on a two-wheel cycle.. BORP: What do you enjoy about BORP?. Ray Ydoyaga: Its great to be able to have a regular and fun outdoor athletic workout after a major physical injury. This wouldnt be possible for me without BORPs special adaptive bikes. BORP is also ideally located at the juncture of multiple bike trails ranging from the very easy loop around Aquatic Park Lake, to hidden paths around Berkeley marina, and to challenging and serious rides up to either the Bay Bridge bike path or, going the other direction, Richmond, and all offering stupendous views. Pre-accident, I was a daily cyclist, so now post-accident, being able to do something physical again that i love has given me a lot of hope and improved my mental well-being.. BORP: Have you noticed a specific impact on ...
Help Cycling 2.5 Gal Betta Tank 276158 - in Freshwater Beginners forum - Hi Everyone, tl;dr Is it really necessary to cycle a 2.5 gallon Betta tank? is this still necessary if all the levels are already fine?...
When compared to other countries The Netherlands has a unique cycling culture. Three years ago I showed you some typically Dutch cycling traits. Mannerisms you certainly wont see in countries with a more racing type of cycling culture. Even in Denmark or Germany, however, the countries with a culture that comes closest to the Dutch,…
This adjustment period is commonly referred to as a fat adaptation phase. I learned about these methods from Dr. Mauro Di Pasquales excellent book: The Metabolic Diet. I learned about "Dr. Di" at a Charles Poliquin training seminar and I later saw him lecture at the SWIS weight training symposium in Toronto, Canada many many years ago.. The Metabolic Diet starts you off on a very low carb "assessment phase" which is what I am describing here.. Why do you need this?. Well, when excessive amounts of poor quality carbohydrates have been over consumed (i.e. diabetes epidemic), insulin levels are chronically elevated which leads to insulin resistance.. Heres an analogy: You walk into a bar (no, this isnt a one liner joke…) and there is a live band playing. You cant hear a thing! Then, eventually, you become kind of numb to the music and it doesnt seem as loud anymore.. Well, thats what happens to the insulin receptors of your cells when you consume an abundance of over processed carbs. Your ...
You are instructed not to make use of or mix it with another GABA boosters including alcohol as mixing these elements with Phenibut may cause several serious
Protein levels of cyclin B1 and cdc2 for each selected population are shown in Fig. 4B. Levels of cyclin B1 protein in cyclin ... Cyclin A regulates the initiation and maintenance of DNA synthesis whereas B cyclins control mitosis (32, 33). Cyclin B mRNA ... Cyclin B1/cdc2 kinase activity is shown in Fig. 4C. Cyclin B1 rescues the p53-dependent drop in cdc2 kinase activity in Ts- ... Cyclin B1 Expression Rescues p53-Mediated G2 Arrest.. To determine whether the decrease in cyclin B1 mRNA was the primary ...
... cyclin-dependent protein serine/threonine kinase regulator activity, protein kinase binding, mitotic cell cycle phase ... transition, regulation of cyclin-dependent protein serine/threonine kinase activity ... cyclin-dependent protein kinase holoenzyme complex, cytoplasm, nucleus, ... IPR039361 Cyclin. IPR013763 Cyclin-like. IPR036915 Cyclin-like_sf. IPR006671 Cyclin_N. ...
Cyclins are positive regulatory subunits of the cyclin-dependent kinases (CDKs), and thereby play an essential role in the ... IPR013763. Cyclin-like. IPR036915. Cyclin-like_sf. IPR015452. Cyclin_B3. IPR004367. Cyclin_C-dom. IPR006671. Cyclin_N. ... IPR013763. Cyclin-like. IPR036915. Cyclin-like_sf. IPR015452. Cyclin_B3. IPR004367. Cyclin_C-dom. IPR006671. Cyclin_N. ... Cluster: G2/mitotic-specific cyclin-B3. 16. Q8WWL7-2. G3RQC9. A0A2I3SM53. A0A2I3H8Y1. F7AMH3. Gorilla gorilla gorilla (Western ...
Compare Cyclin G2 ELISA Kits and find the right product on antibodies-online.com. ... Order Cyclin G2 ELISA Kits for many Reactivities. Chicken, Cow, Dog and more. ... The nucleotide sequence of cyclin G1 and cyclin G2 are 53% identical. Unlike cyclin G1, cyclin G2 contains a C-terminal PEST ... Human Cyclin G2 (CCNG2) interaction partners * This study demonstrates that cyclin G2 suppresses Wnt/beta-catenin signaling and ...
... is a key regulator of the G2/M cell cycle transition. Cyclin B1 accumulates in the cytoplasm through S and G2 phases and ... resulted in nuclear accumulation of cyclin B1 in G2 phase. Disruption of an NES which has been identified in cyclin B1 here ... Nuclear export of cyclin B1 and its possible role in the DNA damage-induced G2 checkpoint.. Toyoshima F1, Moriguchi T, Wada A, ... These results suggest a role of nuclear exclusion of cyclin B1 in the DNA damage-induced G2 checkpoint. ...
Thus, during G2 PP2A activity is high and cyclin B-Cdc2 activity low, thereby preventing phosphorylation of mitotic substrates ... These data are most likely a result of the G2 arrest, although a partial degradation of cyclin B was also observed, probably as ... Loss of human Greatwall results in G2 arrest and multiple mitotic defects due to deregulation of the cyclin B-Cdc2/PP2A balance ... Loss of human Greatwall results in G2 arrest and multiple mitotic defects due to deregulation of the cyclin B-Cdc2/PP2A balance ...
This is the first study of the expression of cyclin G2, a novel cyclin having a role opposite to that of conventional cyclins, ... However, little is known about the cyclin G2 expression in human carcinomas. We thus investigated cyclin G2 expression in human ... retained cyclin G2 expression than carcinomas.. CONCLUSION: Our results suggest that lack of cyclin G2 plays an important role ... Cyclin G2 is a novel cyclin negatively regulating the cell cycle progression, contrary to the characteristics of conventional ...
Whereas many components regulating the progression from S phase through G2 phase into mitosis have been identified, the ... Here we show that depletion of Cyclin A or inhibition of Cdk2 during late S/early G2 phase maintains the G2 phase arrest by ... Thus, a normal role for Cyclin A/Cdk2 during early G2 phase is to increase the level of Cdh1 which destabilises Claspin which ... This mechanism links S phase exit with G2 phase transit into mitosis, provides a novel insight into the roles of Cyclin A/Cdk2 ...
Cyclin G1 and TASCC regulate kidney epithelial cell G2-M arrest and fibrotic maladaptive repair ... Cyclin G1 (CG1), an atypical cyclin, promoted G2-M arrest in PTCs and up-regulated TASCC formation. PTC TASCC formation was ... Cyclin G1 regulates G2-M arrest in proximal tubular cells, promoting a TASCC-induced secretory phenotype, fibrosis, and kidney ... Cyclin G1 regulates G2-M arrest in proximal tubular cells, promoting a TASCC-induced secretory phenotype, fibrosis, and kidney ...
Mitotic G2-G2/M phases (Caenorhabditis elegans) * G2/M Transition (Caenorhabditis elegans) * Cyclin A/B1/B2 associated events ... Cyclin A/B1/B2 associated events during G2/M transition Stable Identifier ... Phosphorylation of Cyclin B1 in the CRS domain (Caenorhabditis elegans) * Translocation of CRS phosphorylated Cyclin B1:Cdc2 ... Formation of Cyclin B:Cdc2 complexes (Caenorhabditis elegans) * Myt-1 mediated phosphorylation of Cyclin B:Cdc2 complexes ( ...
Tong W,Pollard JW,Progesterone inhibits estrogen-induced cyclin D1 and cdk4 nuclear translocation, cyclin E- and cyclin A-cdk2 ... Cyclin B1 binds to Cdc2 at the beginning of G2 phase forming an activated cyclin B1/Cdc2 complex and then phosphorylates its ... Cyclin B1 / biosynthesis, physiology*. Endometrium / cytology*. Female. Flow Cytometry. G2 Phase / physiology*. Humans. Indoles ... cyclin D1 and cyclin E was detected in endometrial carcinomas, which indicated that cyclins might be the major cell cycle ...
Cell cycle control in mammalian cells: role of cyclins, cyclin dependant kinases (CDKs), growth suppressor genes, and cyclin- ... P276-00, a novel cyclin-dependent inhibitor induces G1-G2 arrest, shows antitumor activity on cisplatin-resistant cells and ... Cdk4/6-cyclin D, Cdk2-cyclin E, and the transcription complex that includes pRb and E2F are pivotal in controlling progression ... Hall M, Peters G. genetic alterations of cyclins, cyclin dependent kinases, and Cdk inhibitors in human cancer. Adv Cancer Res ...
Antitumor Imidazolyl Disulfide IV-2 Causes Irreversible G2/M Cell Cycle Arrest without Hyperphosphorylation of Cyclin-Dependent ... Antitumor Imidazolyl Disulfide IV-2 Causes Irreversible G2/M Cell Cycle Arrest without Hyperphosphorylation of Cyclin-Dependent ... Antitumor Imidazolyl Disulfide IV-2 Causes Irreversible G2/M Cell Cycle Arrest without Hyperphosphorylation of Cyclin-Dependent ... Antitumor Imidazolyl Disulfide IV-2 Causes Irreversible G2/M Cell Cycle Arrest without Hyperphosphorylation of Cyclin-Dependent ...
GA-induced G2 or M arrest in glio ... precise expression and activation of several cyclins and cyclin ... GA-induced G2 or M arrest in glioblastoma cells in a cell line-dependent manner. GA decreased the expression of Cdc2 and cyclin ... Geldanamycin induces G2 arrest in U87MG glioblastoma cells through downregulation of Cdc2 and cyclin B1 ... Cdc2 and cyclin B1 were ubiquitinated by GA. MG132 abrogated the GA-induced decrease of Cdc2 and cyclin B1 indicating that ...
Cyclin A was the first cyclin identified (51). Mammals express two A-type cyclins, embryonic-specific cyclin A1 and somatic ... However, cyclin A2 is the major A-type cyclin in somatic cells (52). Cyclin A2 is ubiquitously expressed in proliferating cells ... Loss of cyclin A2 in HDAC10 knockdown cells contributed to G2/M arrest. The effect of HDAC10 on cyclin A2 transcription was ... At late prophase, cyclin A2 may no longer be necessary as cyclin B/CDK1 becomes active, so it is rapidly degraded by the ...
G2- & M-phase Cyclin) Antibody - Without BSA and Azide, Mouse Monoclonal Antibody [Clone V92.1 ] validated in IF, FC, IP ( ... M-phase Cyclin) Antibody - Without BSA and Azide Cyclin B1 (G2- & M-phase Cyclin) Antibody - Without BSA and Azide. Mouse ... Cyclin B1 (G2- & M-phase Cyclin) Antibody - Without BSA and Azide is for research use only and not for use in diagnostic or ... G2/mitotic-specific cyclin-B1, CCNB1, CCNB. Format 200ug/ml of Ab purified from Bioreactor Concentrate by Protein A/G. Prepared ...
These data indicate that the cyclin D3-Cdk4 activity is necessary for cell cycle progression through G2 phase into mitosis and ... Cdk4 and Cdk6 complexes with increased avidity and inhibited a cyclin D3-Cdk4 complex normally activated in late S/early G2 ... Activation of this complex was correlated with the caffeine-induced release from the UV-induced G2 delay and a decrease in the ... The UV-responsive lines contained elevated levels of p16 post-treatment, and the accumulation of p16 correlated with the G2 ...
Chromatin-bound Cdc6 persists in S and G2 phases in human cells, while soluble Cdc6 is destroyed in a cyclin A-cdk2 dependent ... Chromatin-bound Cdc6 persists in S and G2 phases in human cells, while soluble Cdc6 is destroyed in a cyclin A-cdk2 dependent ... Chromatin-bound Cdc6 persists in S and G2 phases in human cells, while soluble Cdc6 is destroyed in a cyclin A-cdk2 dependent ... Chromatin-bound Cdc6 persists in S and G2 phases in human cells, while soluble Cdc6 is destroyed in a cyclin A-cdk2 dependent ...
"CYCLIN-DEPENDENT KINASE G2 regulates salinity stress response and salt mediated flowering in Arabidopsis thaliana, Plant ... CYCLIN-DEPENDENT KINASE G2 regulates salinity stress response and salt mediated flowering in Arabidopsis thaliana. CYCLIN- ... CYCLIN-DEPENDENT KINASE G2 regulates salinity stress response and salt mediated flowering in Arabidopsis thaliana. Ma, Xiaoyan ... Here, Arabidopsis thaliana CYCLIN-DEPENDENT KINASE G2 (CDKG2) was shown to act as a negative regulator of the salinity stress ...
The Disappearance of Cyclins A and B and the Increase in Activity of the G2/M-Phase Cellular Kinase cdc2 in Herpes Simplex ... The levels of cyclin A, cyclin B, and cdc2 decrease in HSV-1-infected cells relative to those of mock-infected cells.The ... Antibodies against cdc2, cyclin A, and cyclin B (Santa Cruz) were diluted 1:100 in PBS. Antibody to MPM-2 (Upstate ... In uninfected cells, peak levels of cyclin A and cyclin B protein were observed at the 12-h time point consistent with expected ...
In the late G2 phase, it is present as an inactive complex of tyrosine-phosphorylated p34cdc2 and unphosphorylated cyclin ... As cells leave the S phase and enter the G2 phase, a massive tyrosine phosphorylation of p34cdc2 occurs. Regulation with ... Meijer L, Azzi L, Wang JY (1991). "Cyclin B targets p34cdc2 for tyrosine phosphorylation". EMBO J. 10 (6): 1545-54. doi:10.1002 ...
The Cdc25 enzymes Cdc25A-C are known to control the transitions from G1 to S phase and G2 to M phase. The structure of Cdc25 ... Cdc25 activates cyclin dependent kinases by removing phosphate from residues in the Cdk active site. In turn, the ... Cyclin "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine. cdc25+ ... May 1991). "Dephosphorylation and activation of a p34cdc2/cyclin B complex in vitro by human CDC25 protein". Nature. 351 (6323 ...
  • More complete depletion correlates with the premature dephosphorylation of cyclin B-Cdc2 substrates, inactivation of the SAC, and subsequent exit from mitosis with severe cytokinesis defects. (pnas.org)
  • Thus, during G2 PP2A activity is high and cyclin B-Cdc2 activity low, thereby preventing phosphorylation of mitotic substrates, whereas at mitotic entry the balance flips, allowing entry into mitosis. (pnas.org)
  • Unlike cyclin B-Cdc2 regulation, very little is known about the mechanisms controlling PP2A activity during mitosis, and therefore our understanding of G2 and mitosis is incomplete. (pnas.org)
  • Whereas many components regulating the progression from S phase through G2 phase into mitosis have been identified, the mechanism by which these components control this critical cell cycle progression is still not fully elucidated. (biomedsearch.com)
  • Cyclin A/Cdk2 has been shown to regulate the timing of Cyclin B/Cdk1 activation and progression into mitosis although the mechanism by which this occurs is only poorly understood. (biomedsearch.com)
  • Thus, a normal role for Cyclin A/Cdk2 during early G2 phase is to increase the level of Cdh1 which destabilises Claspin which in turn down regulates Chk1 activation to allow progression into mitosis. (biomedsearch.com)
  • This mechanism links S phase exit with G2 phase transit into mitosis, provides a novel insight into the roles of Cyclin A/Cdk2 in G2 phase progression, and identifies a novel role for APC/C(Cdh1) in late S/G2 phase cell cycle progression. (biomedsearch.com)
  • These data indicate that the cyclin D3-Cdk4 activity is necessary for cell cycle progression through G2 phase into mitosis and that the increased binding of p16 blocks this activity and G2 phase progression after UV exposure. (garvan.org.au)
  • Essential for the control of the cell cycle at the G2/M (mitosis) transition. (mybiosource.com)
  • G2/M cyclins accumulate steadily during G2 and are abruptly destroyed at mitosis. (mybiosource.com)
  • Involved in the reorganization of the cytoskeleton on transition from G2 to mitosis. (mybiosource.com)
  • Essential for the control of the cell cycle at the G2/M and G1/S (mitosis) transition. (mybiosource.com)
  • 2/mitotic-specific cyclin essential for the control of the cell cycle at the G2/M (mitosis) transition. (mybiosource.com)
  • The kinase that drives mitosis can be modulated by cyclins, by activating phosphorylation, by inhibitory phosphorylation and by binding of inhibitors, but one of these regulatory options controls the transition from G2 phase to mitosis in most circumstances. (nih.gov)
  • A switch-like mechanism integrates signals of cellular status and commits the cell to mitosis by abruptly removing inhibitory phosphate from preformed cyclin:Cdk1 complexes. (nih.gov)
  • The cell cycle consists of four distinct phases: G1 (Gap1) phase, S phase (synthesis), G2 (Gap2) phase (collectively known as interphase) and M phase (mitosis). (wikibooks.org)
  • After S phase or replication cell then enters the G2 phase, which lasts until the cell enters mitosis. (wikibooks.org)
  • Inhibition of protein synthesis during G2 phase prevents the cell from undergoing mitosis. (wikibooks.org)
  • May be involved in the control of the cell cycle at the G1/S (start) and G2/M (mitosis) transitions. (abcam.com)
  • Many G2/M phase-specific genes in plants contain mitosis-specific activator (MSA) elements, which act as G2/M phase-specific enhancers and bind with R1R2R3-Myb transcription factors. (plantphysiol.org)
  • In plants, many G2/M phase-specific genes contain a common cis-acting element, the so-called mitosis-specific activator (MSA) elements ( Ito, 2000 , 2005 ). (plantphysiol.org)
  • Cyclin B1 or CCNB1 is a regulatory protein involved in mitosis. (thermofisher.com)
  • Cyclin B1 is not ubiquitinated during G2/M phase, resulting in its steady accumulation during G2 phase, followed by abrupt APC dependent destruction at the end of mitosis. (thermofisher.com)
  • Mitotic cell cycle progression is accomplished through a reproducible sequence of events, DNA replication (S phase) and mitosis (M phase) separated temporally by gaps (G1 and G2 phases). (genome.jp)
  • Cln1 and Cln2 interacting with Cdc28 promote activation of B-type cyclin associated CDK, which drives DNA replication and entry into mitosis. (genome.jp)
  • After G2, the cell progresses into M phase, mitosis, during which chromosomes condense, and become separated by the mitotic spindle. (madsci.org)
  • Cyclin B1 is the regulatory subunit of the cdc2 kinase and is a protein required for mitotic initiation. (pnas.org)
  • M-phase-promoting factor (MPF), a complex of cdc2 and a B-type cyclin, is a key regulator of the G2/M cell cycle transition. (nih.gov)
  • Here we show that the functional human ortholog of Greatwall protein kinase (Gwl) is the microtubule-associated serine/threonine kinase-like protein, MAST-L. This kinase promotes mitotic entry and maintenance in human cells by inhibiting protein phosphatase 2A (PP2A), a phosphatase that dephosphorylates cyclin B-Cdc2 substrates. (pnas.org)
  • These results suggest that the balance between cyclin B-Cdc2 and PP2A must be tightly regulated for correct mitotic entry and exit and that Gwl is crucial for mediating this regulation in somatic human cells. (pnas.org)
  • In eukaryotic cells, the mitotic state is maintained by the mitotic kinase cyclin B-Cdc2. (pnas.org)
  • Historically, mitotic entry and exit was thought to be the direct consequence of cyclin B-Cdc2 activation and inactivation, respectively ( 1 ). (pnas.org)
  • Specifically, recent evidence indicates that protein phosphatase 2A (PP2A) is responsible for dephosphorylation of cyclin B-Cdc2 substrates and that the regulation of this dephosphorylation is required in mitotic entry and exit ( 3 ). (pnas.org)
  • This finding suggests a previously unexplored model in which the balance between cyclin B-Cdc2 and PP2A controls mitotic entry and exit. (pnas.org)
  • The mechanisms controlling cyclin B-Cdc2 activity have been largely described ( 4 ). (pnas.org)
  • Finally, at mitotic exit cyclin B-Cdc2 is inhibited by the ubiquitin-dependent degradation of its regulatory subunit cyclin B ( 5 ). (pnas.org)
  • Work done in Xenopus egg extracts suggested that Gwl promoted mitotic entry by controlling the auto-amplification loop of cyclin B/Cdc2 ( 8 , 9 ). (pnas.org)
  • However, it has been recently demonstrated that the main role of this kinase is not the regulation of cyclin B-Cdc2 activity but the inhibition of PP2A, the phosphatase that de-phosphorylates cyclin B-Cdc2 substrates ( 10 , 11 ). (pnas.org)
  • To determine the effects of progesterone on the proliferation, cell cycle progression and apoptosis of hECs and to test if cyclin B1 is involved in these effects, progesterone and/or Alsterpaullone (Alp, a specific inhibitor of Cyclin B1/Cdc2) were added to primary hECs. (biomedsearch.com)
  • GA decreased the expression of Cdc2 and cyclin B1 in U87MG cells. (ovid.com)
  • In U251MG cells, the cell cycle was arrested at M phase in addition to G2 by GA. Next, we analyzed the mechanism of the GA-induced regulation of Cdc2 and cyclin B1 in U87MG cells. (ovid.com)
  • Cdc2 and cyclin B1 were ubiquitinated by GA. MG132 abrogated the GA-induced decrease of Cdc2 and cyclin B1 indicating that these proteins were degraded by proteasomes. (ovid.com)
  • In conclusion, GA controls the stability of Cdc2 and cyclin B1 in glioblastomas cell species-dependently. (ovid.com)
  • Cdc2 and cyclin B1 might be responsible for the different responses of glioblastoma cell lines to GA. (ovid.com)
  • In uninfected cells the G 2 /M transition is regulated by cyclin kinase complex containing cdc2 and, initially, cyclin A, followed by cyclin B. cdc2 is downregulated through phosphorylation by wee-1 and myt-1 and upregulated by cdc-25C phosphatase. (asm.org)
  • The activity of cdc2 was higher in infected cell lysates than those of corresponding proteins present in lysates of mock-infected cells even though cyclins A and B were not detectable in lysates of infected cells. (asm.org)
  • vi) The decrease in the levels of cyclins A and B, the increase in activity of cdc2, and the hyperphosphorylation of cdc-25C were mediated by U L 13 and α22/U S 1.5 gene products. (asm.org)
  • Enhanced radiosensitivity by cyclin G1 was correlated with increased cyclin B1, CDC2/cyclin B1 complex, and MPM2. (elsevier.com)
  • Real-time RT-PCR and immunoblotting showed that growth arrest by SmE directly correlates with the reduction of cyclin E, CDK2, CDC25C and CDC2 expression, and up-regulation of p27Kip. (iegt-rostock.de)
  • Cyclin B2 also binds to transforming growth factor beta RII and thus cyclin B2/cdc2 may play a key role in transforming growth factor beta-mediated cell cycle control. (genecards.org)
  • Western blot analysis revealed the increases of cyclin B1 and Cdc2 kinase levels, alone with the decrease of phosphorylated Cdc2 kinase, after treating these cells with the extracts. (hindawi.com)
  • Cyclin B1 complexes with p34 (cdc2) to form the maturation-promoting factor (MPF). (thermofisher.com)
  • The G2-M arrest by silibinin and silymarin was associated with decreased levels of cyclin B1, cyclin A, pCdc2 (Tyr15), Cdc2, and an inhibition of Cdc2 kinase activity. (rti.org)
  • These findings indicate that silymarin and silibinin modulate G1 phase cyclins-CDKs-CDKIs for G1 arrest, and the Chk2-Cdc25C-Cdc2/cyclin B1 pathway for G2-M arrest, together with an altered subcellular localization of critical cell cycle regulators. (rti.org)
  • To identify the mechanism by which p53 regulates G 2 , we have derived a human ovarian cell that undergoes p53-dependent G 2 arrest at 32°C. We have found that p53 prevents G 2 /M transition by decreasing intracellular levels of cyclin B1 protein and attenuating the activity of the cyclin B1 promoter. (pnas.org)
  • To study G 2 regulation by p53, we have established a human cell line, Ts-SKOV3, that stably expresses a temperature-sensitive p53 allele and undergoes G 2 arrest at 32°C. Using this cell line we have found that p53 arrests cell cycle in G 2 by lowering intracellular levels of cyclin B1, a protein absolutely required for mitotic initiation. (pnas.org)
  • Here we show that depletion of Cyclin A or inhibition of Cdk2 during late S/early G2 phase maintains the G2 phase arrest by reducing Cdh1 transcript and protein levels, thereby stabilizing Claspin and maintaining elevated levels of activated Chk1 which contributes to the G2 phase observed. (biomedsearch.com)
  • Involvement of cyclin B1 in progesterone-mediated cell growth inhibition, G2/M cell cycle arrest, and apoptosis in human endometrial cell. (biomedsearch.com)
  • Progesterone may inhibit cell proliferation, mediate G2/M cell cycle arrest and induce apoptosis in hECs via down-regulating Cyclin B1. (biomedsearch.com)
  • GA-induced G2 or M arrest in glioblastoma cells in a cell line-dependent manner. (ovid.com)
  • This cell line showed G2 arrest after GA treatment. (ovid.com)
  • Here, we report that HDAC10 regulates the cell cycle via modulation of cyclin A2 expression, and cyclin A2 overexpression rescues HDAC10 knockdown-induced G 2 /M transition arrest. (asm.org)
  • Unlike conventional cyclins that promote cell cycle progression, cyclin G2 induces G1/S cell cycle arrest even though it possesses a conserved 'cyclin-fold' domain [ 25 ]. (ijbs.com)
  • While it is now well established that inhibition of cyclin/CDK complexes by p21 can result in G1 cell cycle arrest, the consequences of p21/PCNA interaction on cell cycle progression have not yet been determined. (mendeley.com)
  • Here, we show, using a tetracycline-regulated system, that expression of wild-type p21 in p53-deficient DLD1 human colon cancer cells inhibits DNA synthesis and causes G1 and G2 cell cycle arrest. (mendeley.com)
  • Our results suggest that p21 might inhibit cell cycle progression by two independent mechanisms, inhibition of cyclin/CDK complexes, and inhibition of PCNA function resulting in both G1 and G2 arrest. (mendeley.com)
  • Therefore, our data suggest that cyclin G1 enhanced radiation sensitivity by overriding radiation-induced G2 arrest through transcriptional upregulation of cyclin B1. (elsevier.com)
  • Consistently, SmE overexpression leads to inhibition of DNA synthesis and G2 arrest as shown by BrdU-incorporation and MPM2-staining. (iegt-rostock.de)
  • causes a G2 cell cycle arrest by inhibiting CDK1 activity through the regulation of cyclin B1, GADD45A, and BTG2. (viraquest.com)
  • Phenethyl isothiocyanate (PEITC) promotes G2/M phase arrest via p53 expression and induces apoptosis through caspase- and mitochondria-dependent signaling pathways in human prostate cancer DU 145 cells. (qxmd.com)
  • Induction of G2 /M phase arrest and apoptosis of MCF-7 cells by novel benzofuran lignan via suppressing cell cycle proteins]. (qxmd.com)
  • Theaflavins induce G2/M arrest by modulating expression of p21waf1/cip1, cdc25C and cyclin B in human prostate carcinoma PC-3 cells. (qxmd.com)
  • The drug decreased the EWS-FLI1-dependent expression of microtubule stability proteins and of a ubiquitin ligase, which increased the amount of the cell cycle arrest protein cyclin B1, thus promoting mitotic arrest. (sciencemag.org)
  • 6-Gingerol induces cell-cycle G1-phase arrest through AKT-GSK 3β-cyclin D1 pathway in renal-cell carcinoma. (greenmedinfo.com)
  • Further flow cytometric analysis showed that 6-gingerol induced significant G2/M phase arrest and had slight influence on sub-G1 phase in LoVo cells. (hindawi.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)
  • CLB3 ∆ db cells show no cell cycle arrest response to mating pheromone, and CLB3 ∆ db completely bypasses the requirement for CLN G 1 cyclins, even in the absence of the early expressed B-type cyclins CLB5 , 6 . (genetics.org)
  • Determination of DNA content by flow cytometry demonstrated S and G2/M phase arrest of MCF-7 cell, correlated to Cdk1 downregulation, S phase arrest in MDA-MB-231 which is p53 and Cdk1 -dependent, sub-G0 cell cycle arrest in HeLa aligned with Cdk1 downregulation, G0/G1, S, G2/M phase arrest in HepG2 which is p53-dependent. (frontiersin.org)
  • Silymarin and silibinin (50-100 microg/ml) inhibited cell proliferation, induced cell death, and caused G1 and G2-M cell cycle arrest in a dose/time-dependent manner. (rti.org)
  • Molecular studies showed that G1 arrest was associated with a decrease in cyclin D1, cyclin D3, cyclin E, cyclin-dependent kinase (CDK)4, CDK6 and CDK2 protein levels, and CDK2 and CDK4 kinase activity, together with an increase in CDK inhibitors (CDKIs) Kip1/p27 and Cip1/p21. (rti.org)
  • Further, both agents caused cytoplasmic sequestration of cyclin D1 and CDK2, contributing to G1 arrest. (rti.org)
  • Chk2-specific small interfering RNA largely attenuated the silymarin and silibinin-induced G2-M arrest. (rti.org)
  • Plays an important role in controlling cell cycle progression and DNA damage-induced G2 arrest (PubMed:9106657). (rcsb.org)
  • This could arrest tumor growth and promote apoptosis, stopping the cell cycle in G2/M phase. (news-medical.net)
  • Cyclin D associates with Cdk4/Cdk6 and the catalytic activities of the assembled holoenzymes are first manifested by mid-G 1 , increase to a maximum at the G 1 -S transition, and contribute to G 1 exit ( 5 - 8 ). (aacrjournals.org)
  • Cdk2 associates with either cyclin E or cyclin A, and the resultant kinase activities increase at the G 1 -S transition or in the early S phase, respectively. (aacrjournals.org)
  • Collectively, these findings establish WTAP as an essential factor for the stabilization of cyclin A2 mRNA, thereby regulating G 2 /M cell-cycle transition. (elsevier.com)
  • Therefore, cyclins are considered to be the gears that are changed to aid the transition between cycle phases. (omicsonline.org)
  • R-MMU-2565942 (Regulation of PLK1 Activity at G2/M Transition. (ebi.ac.uk)
  • Among its related pathways are Arrhythmogenic right ventricular cardiomyopathy (ARVC) and Regulation of PLK1 Activity at G2/M Transition . (genecards.org)
  • This mitotic kinase complex remains active until the metaphase/anaphase transition when cyclin B is degraded. (fishersci.com)
  • So, cyclin B-p34cdc2 plays a critical role in G2 to M transition. (fishersci.com)
  • Binding to CDK2 leads to CDK2 /cyclin E inactivation at the G1-S phase DNA damage checkpoint, thereby arresting cells at the G1-S transition during DNA repair (PubMed:19445729). (rcsb.org)
  • Cyclin A/Cdk2 regulates Cdh1 and claspin during late S/G2 phase of the cell cycle. (biomedsearch.com)
  • Interestingly, the Cyclin A/Cdk2 regulated APC/C(Cdh1) activity is selective for only a subset of Cdh1 targets including Claspin. (biomedsearch.com)
  • Cdk4/6-cyclin D, Cdk2-cyclin E, and the transcription complex that includes pRb and E2F are pivotal in controlling progression through the late G 1 restriction point ( 9 ). (aacrjournals.org)
  • Recombinant cyclin A-cdk2 can completely substitute for the nucleus in promoting destruction of soluble Xenopus and human Cdc6. (biologists.org)
  • Spliceosomal protein E regulates neoplastic cell growth by modulating expression of cyclin E/CDK2 and G2/M checkpoint proteins. (iegt-rostock.de)
  • We have used biophysical measurements and X-ray crystallography to investigate the ATP-competitive inhibitor binding properties of cyclin-free and cyclin-bound CDK1 and CDK2. (rcsb.org)
  • We conclude that there is a subtle but profound difference between the conformational energy landscapes of cyclin-free CDK1 and CDK2. (rcsb.org)
  • Cyclin E and cdk2 form G1/S-cdk. (brainscape.com)
  • Previously, we found that eIF4A interacts with cyclin-dependent kinase A (CDKA), the plant ortholog of mammalian CDK1. (plantphysiol.org)
  • The cyclin subunit imparts substrate specificity to the complex. (genecards.org)
  • In yeast Cdc28 is the catalytic subunit of the cyclin-dependent kinase (CDK). (genome.jp)
  • Additionally we are shipping Cyclin G2 Antibodies (47) and Cyclin G2 Proteins (3) and many more products for this protein. (antibodies-online.com)
  • Cdc 20 recognizes specific amino acid sequences on M-cyclin and other target proteins. (brainscape.com)
  • One of the up-regulated genes, NtE2C , encoding for cyclin-specific ubiquitin carrier proteins, contained a single functional MSA-like motif, which specifically controlled the expression of a reporter gene in the G2/M phase in BY-2 cells. (plantphysiol.org)
  • Myb proteins in these organisms are present in conserved multiprotein complexes called dREAM or Myb-MuvB, which are involved in the activation of various target genes, including many G2/M phase-specific genes. (plantphysiol.org)
  • In order to be active (able to stick phosphate groups on other proteins) they have to have a partner, called a cyclin. (madsci.org)
  • Cyclin G2 is a novel cyclin negatively regulating the cell cycle progression, contrary to the characteristics of conventional cyclins. (nih.gov)
  • Cell cycle progression in the budding yeast Saccharomyces cerevisiae is controlled by the Cdc28 protein kinase, which is sequentially activated by different sets of cyclins. (mysciencework.com)
  • Taken together, these results indicate that cyclin G2 acts as a tumour suppressor in glioma by repressing glycolysis and tumour progression through its interaction with LDHA. (ijbs.com)
  • The ability of mitotic B-type cyclins to both induce mitotic entry and block mitotic exit may tightly couple many aspects of cell cycle progression to once-per-CDK-cycle ( Nasmyth 1996 ). (genetics.org)
  • Destruction of Cyclin B1 is required for cell cycle progression. (thermofisher.com)
  • HDAC10 regulates cyclin A2 expression by deacetylating histones near the let-7 promoter, thereby repressing transcription. (asm.org)
  • CYCLIN-DEPENDENT KINASE G2 regulates salinity stress response and salt mediated flowering in. (deepdyve.com)
  • Loss of HDAC1 and -2 induces expression of these cyclin-dependent kinase (CDK) inhibitors, leading to a cell cycle block in G 1 . (asm.org)
  • Neisseria meningitidis caused changes in the abundance of several cell cycle regulatory mRNAs, including the cell cycle inhibitors p21(WAF1/CIP1) and cyclin G2 in human brain microvascular endothelial cells. (antibodies-online.com)
  • Furthermore, GSK-3β inhibitors were utilized to explore the role of Wnt/β-catenin signaling in the suppression effect of cyclin G2 on gastric cancer cell proliferation and migration. (biomedcentral.com)
  • Furthermore, GSK-3β inhibitors abolished the cyclin G2-induced suppression of cell proliferation and migration. (biomedcentral.com)
  • A unique feature of p21 that distinguishes it from the other cyclin-dependent kinase (CDK) inhibitors is its ability to associate with the proliferating cell nuclear antigen (PCNA), an auxiliary factor for DNA polymerases delta and epsilon. (mendeley.com)
  • Dysregulation of the cell cycle characterizes many cancer subtypes, providing a rationale for developing cyclin-dependent kinase (CDK) inhibitors. (rcsb.org)
  • Consistent with the requirement for mitotic cyclin degradation for mitotic exit, precise genomic removal of the D box and KEN boxes from the budding yeast mitotic cyclin Clb2 caused a first-cycle block to mitotic exit ( Wäsch and Cross 2002 ). (genetics.org)
  • upon B-type cyclin degradation, no further mitotic entry events occur, but mitotic exit is allowed ( Nasmyth 1996 ). (genetics.org)
  • Cdc14 dephosphorylates Swi5, Sic1, and Cdh1, leading to inhibition of Cdc28 and degradation of cyclin required for mitotic exit. (genome.jp)
  • We found that cyclin G2 levels were decreased in gastric cancer tissues and were associated with tumor size, migration and poor differentiation status. (biomedcentral.com)
  • Treatment of HeLa cells with leptomycin B (LMB), a specific inhibitor of the NES-dependent transport, resulted in nuclear accumulation of cyclin B1 in G2 phase. (nih.gov)
  • Disruption of an NES which has been identified in cyclin B1 here abolished the nuclear export of this protein, and consequently the NES-disrupted cyclin B1 when expressed in cells accumulated in the nucleus. (nih.gov)
  • Moreover, we show that expression of the NES-disrupted cyclin B1 or LMB treatment of the cells is able to override the DNA damage-induced G2 checkpoint when combined with caffeine treatment. (nih.gov)
  • The complete depletion of Gwl by siRNA arrests human cells in G2. (pnas.org)
  • Normal thyroids expressed cyclin G2 in more than 5% of follicular cells. (nih.gov)
  • Of 30 papillary carcinomas including 6 microcarcinoma, cyclin G2 expression was not, or only occasionally, observed in carcinoma cells, indicating its expression decreased in all these cases. (nih.gov)
  • On the other hand, in 16 of the 24 follicular adenomas (66.7%) and 5 of the 23 follicular carcinomas (21.7%), cyclin G2 expression was retained (more than 5% of neoplastic cells were positive), and adenomas more frequently (p = 0.0032) retained cyclin G2 expression than carcinomas. (nih.gov)
  • Thus, substitution of aspartic acid 199 with alanine in ICP0 abolished stabilization of cyclin D3, reduced the yields of virus from resting cells, and reduced the capacity of the virus to invade the mouse central nervous system from a peripheral site. (asm.org)
  • Here we report that in UV-irradiated HeLa and A2058 cells, p16 bound Cdk4 and Cdk6 complexes with increased avidity and inhibited a cyclin D3-Cdk4 complex normally activated in late S/early G2 phase. (garvan.org.au)
  • Finally, overexpression of a dominant-negative mutant of Cdk4 blocked cells in G2 phase. (garvan.org.au)
  • The consequences of this negative regulation were most apparent in clb6 mutants, which had a shorter pre-Start G1 phase as well as a shorter G2 phase than congenic wild-type cells. (mysciencework.com)
  • Furthermore, specific inactivation of SmE by shRNA significantly increased the percentage of cells in S phase, whereas the amount of G2/M arrested cells was reduced. (iegt-rostock.de)
  • These cells do not express any G1 cyclins (clns). (slideserve.com)
  • Combined microarray data from transgenic lines and synchronized cells revealed that overexpression of the truncated hyperactive form of NtmybA2, but not its full-length form, preferentially up-regulated many G2/M phase-specific genes in BY-2 cells. (plantphysiol.org)
  • HN30 cells are from head and neck cancer tumors that over express cyclin B1 and D1. (antibodies-online.com)
  • During G2, the cells "check" the DNA to make sure no mistakes were made. (madsci.org)
  • Quantitative analysis demonstrated that the number of cells with cytoplasmic cyclin B localization increased in a very similar fashion. (jci.org)
  • At higher stoichiometric ratios, inhibits the kinase activity of the cyclin D- CDK4 complex. (rcsb.org)
  • Thus, the in vitro cellular potency, together with in vivo antitumor activity, confirms the potential of P276-00, a cyclin-dependent kinase inhibitor as an anticancer molecule. (aacrjournals.org)
  • HMGA2 loss resulted in enrichment of the transcriptional repressor E4F at the cyclin A2 promoter. (asm.org)
  • In contrast to the E2F-dependent regulation of G1/S phase-specific genes, less is known about the transcriptional regulation of genes expressed at the G2/M phase. (plantphysiol.org)
  • Moreover, overexpression of cyclin G2 attenuated tumor growth and metastasis both in vitro and in vivo. (biomedcentral.com)
  • WTAP knockdown induced G 2 accumulation, which is partially rescued by adenoviral overexpression of cyclin A2. (elsevier.com)
  • Overexpression of cyclin G1 was observable in lung carcinoma tissues. (elsevier.com)
  • Therefore, we propose that the transcription of many G2/M phase-specific genes in tobacco is positively regulated by NtmybA2, in most cases through direct binding to the MSA elements. (plantphysiol.org)
  • The myb3r1 myb3r4 double mutant showed decreased expression of G2/M phase-specific genes, including CYCB2;1 , CDC20.1 , and KNOLLE ( KN ). (plantphysiol.org)
  • On the other hand, deletion of many cyclin genes leads to, at most, minor defects. (genetics.org)
  • Notably, these mutations do not effect transcription of other spermatocyte genes, such as pelota, cyclin A and roughex . (biologists.org)
  • Cyclin B1 accumulates in the cytoplasm through S and G2 phases and translocates to the nucleus during prophase. (nih.gov)
  • Expression increases in early G1 phase and reaches highest levels during the S and G2/M phases. (abcam.com)
  • G1, S, and G2 phases are collectively known as interphase. (genome.jp)
  • a. start with cdk 4/6 (inactive) with inhibitor phosphate b. mitogen through Ras activated cyclin D c. cyclin D binds to cdk 4/6 d. add cak with activating phosphate e. lose inhibitor phosphate f. (brainscape.com)
  • abstract = "Although cyclin G1 has been implicated in certain p53-related biological phenomena, other aspects of its function remain unclear. (elsevier.com)
  • Previous work in many organisms has indicated that B-type cyclin-dependent inhibition of mitotic exit imposes a requirement for mitotic destruction of B-type cyclins. (genetics.org)
  • This is the first study of the expression of cyclin G2, a novel cyclin having a role opposite to that of conventional cyclins, in human carcinoma. (nih.gov)
  • CONCLUSION: Our findings suggest that cyclin B1 is a critical factor in proliferation and differentiation of hECs. (biomedsearch.com)
  • Activation of the mitotic kinase during G2 causes repression of CLN1, CLN2 and CLN3 synthesis and onset of M phase and ultimately leads to the reactivation of CLB proteolysis. (slideserve.com)
  • The inactive cyclin B-p34cdc2 complex continues to accumulate in the cytoplasm until the completion of DNA synthesis, when Cdc25, a specific protein phosphatase, dephosphorylates aa 14Thr and 15Tyr of p34cdc2 rendering the complex active at the G2/M boundary. (fishersci.com)
  • Nevertheless, both Clb5 and Clb6 were shown to be responsible for down-regulation of the protein kinase activities associated with Cln2, a G1 cyclin, and Clb2, a mitotic cyclin, in vivo. (mysciencework.com)
  • If one removes methionine, Cln2 (the G1 cyclin) is made. (slideserve.com)
  • METHODS: To investigate the role of cyclin B1 in proliferation and differentiation of hECs in menstrual cycle, the expression of cyclin B1 throughout the menstrual cycle was evaluated in hECs. (biomedsearch.com)
  • We show here that cytoplasmic localization of cyclin B1 during interphase is directed by its nuclear export signal (NES)-dependent transport mechanism. (nih.gov)
  • Decreased expression of cyclin G2 is significantly linked to the malignant transformation of papillary carcinoma of the thyroid. (nih.gov)
  • However, little is known about the cyclin G2 expression in human carcinomas. (nih.gov)
  • We thus investigated cyclin G2 expression in human thyroid neoplasms. (nih.gov)
  • We immunohistochemically examined cyclin G2 expression in 40 normal thyroids and 80 thyroid neoplasms. (nih.gov)
  • Real-time PCR, immunohistochemistry and in silico assay were used to determine the expression of cyclin G2 in gastric cancer. (biomedcentral.com)
  • TCGA datasets were used to evaluate the association between cyclin G2 expression and the prognostic landscape of gastric cancers. (biomedcentral.com)
  • The effects of cyclin G2 expression on Wnt/β-catenin signaling were explored using a TOPFlash luciferase reporter assay, and the molecular mechanisms involved were investigated using immunoblots assay, yeast two-hybrid screening, immunoprecipitation and Duolink in situ PLA. (biomedcentral.com)
  • Dpr1 was identified as a cyclin G2-interacting protein which was required for the cyclin G2-mediated inhibition of β-catenin expression. (biomedcentral.com)
  • We evaluated the role of miR-122 and cyclin G1 expression in hepatocarcinogenesis and in response to treatment with doxorubicin and their relevance on survival and time to recurrence (TTR) of HCC patients. (aacrjournals.org)
  • In addition, in a therapeutic perspective, we assayed the effects of a restored miR-122 expression in triggering doxorubicin-induced apoptosis and we proved that miR-122, as well as cyclin G1 silencing, increases sensitivity to doxorubicin challenge. (aacrjournals.org)
  • In patients resected for HCC, lower miR-122 levels were associated with a shorter TTR, whereas higher cyclin G1 expression was related to a lower survival, suggesting that miR-122 might represent an effective molecular target for HCC. (aacrjournals.org)
  • Cyclin G2 has been shown to be associated with the development of multiple types of tumors, but its underlying mechanisms in gastric tumors is not well-understood. (biomedcentral.com)
  • The aim of this study is to investigate the role and the underlying mechanisms of cyclin G2 on Wnt/β-catenin signaling in gastric cancer. (biomedcentral.com)
  • Moreover, a xenograft model and a metastasis model of nude mice was used to determine the influence of cyclin G2 on gastric tumor growth and migration in vivo. (biomedcentral.com)
  • However, there are few reports on the identity of pathways and the precise mechanisms that mediate the roles of cyclin G2 in gastric tumorigenesis and other cancers. (biomedcentral.com)