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.

Control of cell cycle progression by c-Jun is p53 dependent. (1/114)

The c-jun proto-oncogene encodes a component of the mitogen-inducible immediate-early transcription factor AP-1 and has been implicated as a positive regulator of cell proliferation and G1-to-S-phase progression. Here we report that fibroblasts derived from c-jun-/- mouse fetuses exhibit a severe proliferation defect and undergo a prolonged crisis before spontaneous immortalization. The cyclin D1- and cyclin E-dependent kinases (CDKs) and transcription factor E2F are poorly activated, resulting in inefficient G1-to-S-phase progression. Furthermore, the absence of c-Jun results in elevated expression of the tumor suppressor gene p53 and its target gene, the CDK inhibitor p21, whereas overexpression of c-Jun represses p53 and p21 expression and accelerates cell proliferation. Surprisingly, protein stabilization, the common mechanism of p53 regulation, is not involved in up-regulation of p53 in c-jun-/- fibroblasts. Rather, c-Jun regulates transcription of p53 negatively by direct binding to a variant AP-1 site in the p53 promoter. Importantly, deletion of p53 abrogates all defects of cells lacking c-Jun in cell cycle progression, proliferation, immortalization, and activation of G1 CDKs and E2F. These results demonstrate that an essential, rate-limiting function of c-Jun in fibroblast proliferation is negative regulation of p53 expression, and establish a mechanistic link between c-Jun-dependent mitogenic signaling and cell-cycle regulation.  (+info)

Altered regulation of cyclin G in human breast cancer and its specific localization at replication foci in response to DNA damage in p53+/+ cells. (2/114)

Cyclin G, a recent addition to the cyclin family, was initially identified in screens for new src kinase family members and soon thereafter by differential screening for transcriptional targets of the tumor suppressor gene, p53. We have identified cyclin G as being overexpressed in breast and prostate cancer cells using differential display polymerase chain reaction screening. We demonstrate here that cyclin G is overexpressed in human breast and prostate cancer cells and in cancer cells in situ from tumor specimens. Cyclin G expression was tightly regulated throughout the cell cycle in normal breast cells, peaking at the S and G2/M phases of the cell cycle with lower levels in G1. The cell cycle-dependent expression was absent in breast cancer cells. Following DNA damage in normal p53+/+ cells, cyclin G is triggered to cluster in discrete nuclear DNA replication foci that contain replication-associated proteins such as proliferating cell nuclear antigen (PCNA). While p53-/- cells displayed a faint cyclin G nuclear staining pattern, there was no increased expression and no change in distribution of the staining pattern after DNA damage. The specific subcellular localization of cyclin G at DNA replication foci provides an additional link between p53-mediated growth arrest and cell cycle regulation and suggests that cyclin G may act as an effector of p53-mediated events by functional association with replication foci protein(s).  (+info)

A G1 cyclin is necessary for maintenance of filamentous growth in Candida albicans. (3/114)

Candida albicans undergoes a dramatic morphological transition in response to various growth conditions. This ability to switch from a yeast form to a hyphal form is required for its pathogenicity. The intractability of Candida to traditional genetic approaches has hampered the study of the molecular mechanism governing this developmental switch. Our approach is to use the more genetically tractable yeast Saccharomyces cerevisiae to yield clues about the molecular control of filamentation for further studies in Candida. G1 cyclins Cln1 and Cln2 have been implicated in the control of morphogenesis in S. cerevisiae. We show that C. albicans CLN1 (CaCLN1) has the same cell cycle-specific expression pattern as CLN1 and CLN2 of S. cerevisiae. To investigate whether G1 cyclins are similarly involved in the regulation of cell morphogenesis during the yeast-to-hypha transition of C. albicans, we mutated CaCLN1. Cacln1/Cacln1 cells were found to be slower than wild-type cells in cell cycle progression. The Cacln1/Cacln1 mutants were also defective in hyphal colony formation on several solid media. Furthermore, while mutant strains developed germ tubes under several hypha-inducing conditions, they were unable to maintain the hyphal growth mode in a synthetic hypha-inducing liquid medium and were deficient in the expression of hypha-specific genes in this medium. Our results suggest that CaCln1 may coordinately regulate hyphal development with signal transduction pathways in response to various environmental cues.  (+info)

G1 checkpoint protein and p53 abnormalities occur in most invasive transitional cell carcinomas of the urinary bladder. (4/114)

The G1 cell cycle checkpoint regulates entry into S phase for normal cells. Components of the G1 checkpoint, including retinoblastoma (Rb) protein, cyclin D1 and p16INK4a, are commonly altered in human malignancies, abrogating cell cycle control. Using immunohistochemistry, we examined 79 invasive transitional cell carcinomas of the urinary bladder treated by cystectomy, for loss of Rb or p16INK4a protein and for cyclin D1 overexpression. As p53 is also involved in cell cycle control, its expression was studied as well. Rb protein loss occurred in 23/79 cases (29%); it was inversely correlated with loss of p16INK4a, which occurred in 15/79 cases (19%). One biphenotypic case, with Rb+p16- and Rb-p16+ areas, was identified as well. Cyclin D1 was overexpressed in 21/79 carcinomas (27%), all of which retained Rb protein. Fifty of 79 tumours (63%) showed aberrant accumulation of p53 protein; p53 staining did not correlate with Rb, p16INK4a, or cyclin D1 status. Overall, 70% of bladder carcinomas showed abnormalities in one or more of the intrinsic proteins of the G1 checkpoint (Rb, p16INK4a and cyclin D1). Only 15% of all bladder carcinomas (12/79) showed a normal phenotype for all four proteins. In a multivariate survival analysis, cyclin D1 overexpression was linked to less aggressive disease and relatively favourable outcome. In our series, Rb, p16INK4a and p53 status did not reach statistical significance as prognostic factors. In conclusion, G1 restriction point defects can be identified in the majority of bladder carcinomas. Our findings support the hypothesis that cyclin D1 and p16INK4a can cooperate to dysregulate the cell cycle, but that loss of Rb protein abolishes the G1 checkpoint completely, removing any selective advantage for cells that alter additional cell cycle proteins.  (+info)

Recovery of the yeast cell cycle from heat shock-induced G(1) arrest involves a positive regulation of G(1) cyclin expression by the S phase cyclin Clb5. (5/114)

In the yeast Saccharomyces cerevisiae, heat shock stress induces a variety of cellular responses including a transient cell cycle arrest before G(1)/S transition. Previous studies have suggested that this G(1) delay is probably attributable to a reduced level of the G(1) cyclin gene (CLN1 and CLN2) transcripts. Here we report our finding that the G(1) cyclin Cln3 and the S cyclin Clb5 are the key factors required for recovery from heat shock-induced G(1) arrest. Heat shock treatment of G(1) cells lacking either CLN3 or CLB5/CLB6 functions leads to prolonged cell cycle arrest before the initiation of DNA synthesis, concomitant with a severe deficiency in bud formation. The inability of the clb5 clb6 mutant to resume normal budding after heat shock treatment is unanticipated, since the S phase cyclins are generally thought to be required mainly for initiation of DNA synthesis and have no significant roles in bud formation in the presence of functional G(1) cyclins. Further studies reveal that the accumulation of G(1) cyclin transcripts is markedly delayed in the clb5 clb6 mutant following heat shock treatment, indicating that the CLN gene expression may require Clb5/Clb6 to attain a threshold level for driving the cell cycle through G(1)/S transition. Consistent with this assumption, overproduction of Clb5 greatly enhances the transcription of at least two G(1) cyclin genes (CLN1 and CLN2) in heat-shocked G(1) cells. These results suggest that Clb5 may positively regulate the expression of G(1) cyclins during cellular recovery from heat shock-induced G(1) arrest. Additional evidence is presented to support a role for Clb5 in maintaining the synchrony between budding and DNA synthesis during normal cell division as well.  (+info)

Ectopic expression of Cdc25A accelerates the G(1)/S transition and leads to premature activation of cyclin E- and cyclin A-dependent kinases. (6/114)

Human Cdc25 phosphatases play important roles in cell cycle regulation by removing inhibitory phosphates from tyrosine and threonine residues of cyclin-dependent kinases. Three human Cdc25 isoforms, A, B, and C, have been discovered. Cdc25B and Cdc25C play crucial roles at the G(2)/M transition. In the present study, we have investigated the function of human Cdc25A phosphatase. Cell lines that express human Cdc25A in an inducible manner have been generated. Ectopic expression of Cdc25A accelerates the G(1)/S-phase transition, indicating that Cdc25A controls an event(s) that is rate limiting for entry into S phase. Furthermore, we carried out a detailed analysis of the expression and activation of human Cdc25A. Activation of endogenous Cdc25A occurs during late G(1) phase and increases in S and G(2) phases. We further demonstrate that Cdc25A is activated at the same time as cyclin E- and cyclin A-dependent kinases. In vitro, Cdc25A dephosphorylates and activates the cyclin-Cdk complexes that are active during G(1). Overexpression of Cdc25A in the inducible system, however, leads to a premature activation of both cyclin E-Cdk2 and cyclin A-Cdk2 complexes, while no effect of cyclin D-dependent kinases is observed. Furthermore, Cdc25A overexpression induces a tyrosine dephosphorylation of Cdk2. These results suggest that Cdc25A is an important regulator of the G(1)/S-phase transition and that cyclin E- and cyclin A-dependent kinases act as direct targets.  (+info)

A role of cyclin G in the process of apoptosis. (7/114)

Cyclin G was previously identified as a target gene of the p53 tumor suppresser protein, and levels of cyclin G are increased after induction of p53 by DNA damage. However, the function of cyclin G has not been established. To determine the effect of increased expression of cyclin G, retroviruses encoding cyclin G were constructed and used to infect three different murine cell lines. Cyclin G protein levels induced by the retroviruses were within the range seen after DNA damage induction of p53. In each case we observed that such over-expression of cyclin G augments the apoptotic process. TNF-alpha induction of apoptosis is increased by expression of cyclin G in NIH3T3 fibroblasts which express p53, as well as in 10.1 fibroblasts which contain no p53 allele. Additionally, we observed that while cyclin G expression is markedly reduced upon aggregate formation in embryonic carcinoma P19 cells, retrovirus-mediated over-expression of cyclin G enhances apoptotic cell death in aggregated P19 cells, and increases the extent of apoptosis caused by retinoic acid or serum starvation of these cells. These data demonstrate that cyclin G plays a facilitating role in modulating apoptosis induced by different stimuli. Moreover, we have discovered that cyclin G expression is rapidly induced in P19 cells after exposure to Bone Morphogenic Protein-4 (BMP-4), suggesting that cyclin G may mediate apoptotic signals generated by BMP-4.  (+info)

Interferon-alpha inhibits proliferation in human T lymphocytes by abrogation of interleukin 2-induced changes in cell cycle-regulatory proteins. (8/114)

IFN-alpha exerts prominent regulatory functions on the immune system. One such effect is the inhibition of proliferation of in vitro stimulated T lymphocytes. The exact physiological function of this activity is not known, but it has been implicated in the antiviral effects of IFN, its antitumor action in T-cell malignancies, and the regulation of the in vivo T-cell response. Here, we have investigated the mechanism underlying the IFN-alpha-mediated growth inhibition of normal human PHA- and IL-2-stimulated T lymphocytes by an analysis of how IFN-alpha treatment influences known molecular events that normally accompany the transition from quiescence to proliferation in these cells. IFN-alpha treatment was found to profoundly block S-phase entry of stimulated T lymphocytes. This correlated with a strong inhibition of IL-2-induced changes in G1-regulatory proteins, including the prevented up-regulation of G1 cyclins and cyclin-dependent kinases as well as an abrogation of mitogen-induced reduction of p27Kip1 levels. This latter effect was due to a maintained stability of the p27Kip1 protein in the IFN-alpha-treated cells. In line with these findings, phosphorylation of the pocket proteins was abrogated in IFN-alpha-treated cells. Furthermore, our data indicate that IFN-alpha has selective effects on the pathways that emerge from the IL-2 receptor because IFN-alpha treatment does not block IL-2-induced up-regulation of c-myc or Cdc25A.  (+info)

Cyclin G1 is a type of protein that belongs to the cyclin family, which are involved in the regulation of the cell cycle. The cell cycle is the series of events that take place as a cell grows, copies its DNA, and divides into two daughter cells.

Cyclin G1 regulates the cell cycle by interacting with various cyclin-dependent kinases (CDKs), which are enzymes that help control the progression of the cell cycle. Specifically, Cyclin G1 has been shown to inhibit the activity of CDK1 and CDK2, which play important roles in regulating the transition from the G1 phase to the S phase of the cell cycle.

Cyclin G1 has also been implicated in other cellular processes, including DNA damage repair, apoptosis (programmed cell death), and tumor suppression. Dysregulation of Cyclin G1 has been linked to various types of cancer, making it a potential target for cancer therapy.

Cyclin G is a type of protein that belongs to the cyclin family, which are involved in the regulation of the cell cycle. The human Cyclin G gene encodes two isoforms, Cyclin G1 and Cyclin G2, which share a similar structure but have different functions.

Cyclin G1 is known to play a role in the negative regulation of the cell cycle, particularly during the G1 phase. It interacts with several proteins, including CDKs (cyclin-dependent kinases), to regulate the activity of various transcription factors and other signaling pathways that control cell growth and division.

Cyclin G2, on the other hand, has been implicated in the regulation of DNA damage response and apoptosis (programmed cell death). It interacts with CDKs and other proteins to modulate the activity of various signaling pathways involved in these processes.

Overall, Cyclin G plays important roles in regulating cell cycle progression, DNA damage response, and apoptosis, and its dysregulation has been linked to several human diseases, including cancer.

Cyclin D1 is a type of cyclin protein that plays a crucial role in the regulation of the cell cycle, which is the process by which cells divide and grow. Specifically, Cyclin D1 is involved in the transition from the G1 phase to the S phase of the cell cycle. It does this by forming a complex with and acting as a regulatory subunit of cyclin-dependent kinase 4 (CDK4) or CDK6, which phosphorylates and inactivates the retinoblastoma protein (pRb). This allows the E2F transcription factors to be released and activate the transcription of genes required for DNA replication and cell cycle progression.

Overexpression of Cyclin D1 has been implicated in the development of various types of cancer, as it can lead to uncontrolled cell growth and division. Therefore, Cyclin D1 is an important target for cancer therapy, and inhibitors of CDK4/6 have been developed to treat certain types of cancer that overexpress Cyclin D1.

Cyclin A is a type of cyclin protein that regulates the progression of the cell cycle, particularly through the G1 and S phases. It forms a complex with and acts as a regulatory subunit for cyclin-dependent kinases (CDKs), specifically CDK2 and CDK1. The activation of Cyclin A-CDK complexes leads to phosphorylation of various target proteins, which in turn regulates DNA replication and the transition to mitosis.

Cyclin A levels rise during the late G1 phase and peak during the S phase, after which they decline rapidly during the G2 phase. Any abnormalities in Cyclin A regulation or expression can contribute to uncontrolled cell growth and cancer development.

Cyclin E is a type of cyclin protein that plays a crucial role in the regulation of the cell cycle, particularly during the G1 phase and the transition to the S phase. It functions as a regulatory subunit of the Cyclin-dependent kinase 2 (CDK2) complex, which is responsible for promoting the progression of the cell cycle.

Cyclin E is synthesized during the late G1 phase of the cell cycle and accumulates to high levels until it forms a complex with CDK2. The Cyclin E-CDK2 complex then phosphorylates several target proteins, leading to the activation of various downstream pathways that promote DNA replication and cell cycle progression.

The regulation of Cyclin E expression and activity is tightly controlled through multiple mechanisms, including transcriptional regulation, protein stability, and proteasomal degradation. Dysregulation of Cyclin E has been implicated in various human cancers, including breast, ovarian, and lung cancer, due to its role in promoting uncontrolled cell proliferation and genomic instability.

Cyclin B is a type of cyclin protein that regulates the cell cycle, specifically the transition from G2 phase to mitosis (M phase) in eukaryotic cells. Cyclin B binds and activates cyclin-dependent kinase 1 (CDK1), forming the complex known as M-phase promoting factor (MPF). This complex triggers the events leading to cell division, such as chromosome condensation, nuclear envelope breakdown, and spindle formation. The levels of cyclin B increase during the G2 phase and are degraded by the anaphase-promoting complex/cyclosome (APC/C) at the onset of anaphase, allowing the cell cycle to progress into the next phase.

Cyclin B1 is a type of cyclin protein that regulates the cell cycle, specifically the transition from G2 phase to mitosis (M phase) in eukaryotic cells. It forms a complex with and acts as a regulatory subunit of cyclin-dependent kinase 1 (CDK1), also known as CDC2. During the G2 phase, Cyclin B1 levels accumulate and upon reaching a certain threshold, it binds to CDK1 to form the maturation promoting factor (MPF). The activation of MPF triggers the onset of mitosis by promoting nuclear envelope breakdown, chromosome condensation, and other events required for cell division. After the completion of mitosis, Cyclin B1 is degraded by the ubiquitin-proteasome system, allowing the cell cycle to progress back into G1 phase.

Cyclin D2 is a type of cyclin protein that regulates the cell cycle, particularly in the G1 phase. It forms a complex with and acts as a regulatory subunit of cyclin-dependent kinase 4 (CDK4) or CDK6, promoting the transition from G1 to S phase of the cell cycle. The expression of cyclin D2 is regulated by various growth factors, hormones, and oncogenes, and its dysregulation has been implicated in the development of several types of cancer.

Cyclin D3 is a type of cyclin protein that regulates the cell cycle, particularly during the G1 phase. It forms a complex with and acts as a regulatory subunit of CDK4 or CDK6, which are cyclin-dependent kinases. This complex plays a crucial role in phosphorylating and inactivating the retinoblastoma protein (pRb), leading to the release of E2F transcription factors that promote the expression of genes required for DNA replication and cell cycle progression into the S phase.

Cyclin D3 is primarily expressed in activated lymphocytes and is essential for normal immune function, as well as in certain tissues during development. Alterations in CYCLIN D3 gene expression or function have been implicated in several types of cancer, such as leukemias and lymphomas, due to their role in uncontrolled cell proliferation.

Cyclin A1 is a type of cyclin protein that regulates the cell cycle, particularly during the S and G2 phases. It forms a complex with and acts as a regulatory subunit of cyclin-dependent kinase 2 (CDK2), helping to control the transition from the G1 phase to the S phase and from the S phase to the G2 phase. Cyclin A1 is expressed in various tissues, including ovary, testis, bone marrow, and lymphoid cells. Overexpression or dysregulation of cyclin A1 has been implicated in several types of cancer, making it a potential target for cancer therapy.

Cyclins are a family of regulatory proteins that play a crucial role in the cell cycle, which is the series of events that take place as a cell grows, divides, and produces two daughter cells. They are called cyclins because their levels fluctuate or cycle during the different stages of the cell cycle.

Cyclins function as subunits of serine/threonine protein kinase complexes, forming an active enzyme that adds phosphate groups to other proteins, thereby modifying their activity. This post-translational modification is a critical mechanism for controlling various cellular processes, including the regulation of the cell cycle.

There are several types of cyclins (A, B, D, and E), each of which is active during specific phases of the cell cycle:

1. Cyclin D: Expressed in the G1 phase, it helps to initiate the cell cycle by activating cyclin-dependent kinases (CDKs) that promote progression through the G1 restriction point.
2. Cyclin E: Active during late G1 and early S phases, it forms a complex with CDK2 to regulate the transition from G1 to S phase, where DNA replication occurs.
3. Cyclin A: Expressed in the S and G2 phases, it associates with both CDK2 and CDK1 to control the progression through the S and G2 phases and entry into mitosis (M phase).
4. Cyclin B: Active during late G2 and M phases, it partners with CDK1 to regulate the onset of mitosis by controlling the breakdown of the nuclear envelope, chromosome condensation, and spindle formation.

The activity of cyclins is tightly controlled through several mechanisms, including transcriptional regulation, protein degradation, and phosphorylation/dephosphorylation events. Dysregulation of cyclin expression or function can lead to uncontrolled cell growth and proliferation, which are hallmarks of cancer.

Cyclin A2 is a type of cyclin protein that regulates the cell cycle, which is the series of events that cells undergo as they grow and divide. Specifically, Cyclin A2 plays a role in the progression from the G1 phase to the S phase (DNA synthesis phase) and from the G2 phase to the M phase (mitosis phase) of the cell cycle. It does this by binding to and activating cyclin-dependent kinases (CDKs), which are enzymes that help regulate the cell cycle.

Cyclin A2 is expressed at various points during the cell cycle, but its levels peak during the S and G2 phases. The protein is degraded during mitosis, ensuring that it is not present in excess during the next cell cycle. Dysregulation of Cyclin A2 has been implicated in the development of cancer, as uncontrolled cell growth and division are hallmarks of this disease.

Cyclin D is a type of cyclin protein that plays a crucial role in the regulation of the cell cycle, which is the process by which cells grow and divide. Specifically, Cyclin D is involved in the G1 phase of the cell cycle and works in conjunction with its partner enzyme, cyclin-dependent kinase 4 (CDK4) or CDK6, to phosphorylate and regulate the activity of several key proteins that control the transition from G1 to S phase.

There are several different types of Cyclin D proteins, including Cyclin D1, Cyclin D2, and Cyclin D3, which are encoded by different genes but share similar structures and functions. Overexpression or dysregulation of Cyclin D has been implicated in the development of various human cancers, as it can lead to uncontrolled cell growth and division. Therefore, understanding the role of Cyclin D in the cell cycle and its regulation is important for developing potential cancer therapies.

Cyclin G2 is a type of protein that belongs to the cyclin family, which are involved in the regulation of the cell cycle. The cell cycle is the series of events that cells undergo as they grow and divide. Specifically, Cyclin G2 regulates the G1 phase of the cell cycle, which is the phase where the cell prepares to divide.

Cyclin G2 has been found to play a role in several important cellular processes, including DNA damage response, apoptosis (programmed cell death), and differentiation. It has also been implicated in the development of certain diseases, such as cancer. For example, Cyclin G2 has been shown to have tumor-suppressive functions, and its expression is often reduced in cancer cells.

In summary, Cyclin G2 is a regulatory protein that plays a critical role in controlling the cell cycle and maintaining genomic stability. Its dysregulation has been associated with various diseases, including cancer.

Cyclin C is a type of cyclin protein that plays a crucial role in the regulation of the cell cycle, which is the process by which cells grow and divide. Specifically, Cyclin C is involved in the transition from the G1 phase to the S phase of the cell cycle, during which DNA replication occurs.

Cyclin C forms a complex with cyclin-dependent kinase 8 (CDK8) and other regulatory subunits to form the CDK8 module, which is part of the mediator complex that regulates gene transcription. The activity of Cyclin C/CDK8 is regulated by various mechanisms, including phosphorylation and degradation, to ensure proper control of the cell cycle and prevent uncontrolled cell growth and division.

Mutations in the gene encoding Cyclin C have been associated with certain types of cancer, highlighting its importance in maintaining genomic stability and preventing tumorigenesis.

The cell cycle is a series of events that take place in a cell leading to its division and duplication. It consists of four main phases: G1 phase, S phase, G2 phase, and M phase.

During the G1 phase, the cell grows in size and synthesizes mRNA and proteins in preparation for DNA replication. In the S phase, the cell's DNA is copied, resulting in two complete sets of chromosomes. During the G2 phase, the cell continues to grow and produces more proteins and organelles necessary for cell division.

The M phase is the final stage of the cell cycle and consists of mitosis (nuclear division) and cytokinesis (cytoplasmic division). Mitosis results in two genetically identical daughter nuclei, while cytokinesis divides the cytoplasm and creates two separate daughter cells.

The cell cycle is regulated by various checkpoints that ensure the proper completion of each phase before progressing to the next. These checkpoints help prevent errors in DNA replication and division, which can lead to mutations and cancer.

Cyclin-dependent kinases (CDKs) are a family of serine/threonine protein kinases that play crucial roles in regulating the cell cycle, transcription, and other cellular processes. They are activated by binding to cyclin proteins, which accumulate and degrade at specific stages of the cell cycle. The activation of CDKs leads to phosphorylation of various downstream target proteins, resulting in the promotion or inhibition of different cell cycle events. Dysregulation of CDKs has been implicated in several human diseases, including cancer, and they are considered important targets for drug development.

Cyclin B2 is a type of cyclin protein that regulates the cell cycle, particularly at the G2 phase and the beginning of mitosis. It forms a complex with and acts as a regulatory subunit of cyclin-dependent kinase 1 (CDK1), which plays a crucial role in the transition from G2 phase to mitosis. The expression and activity of Cyclin B2 are tightly regulated during the cell cycle, and its dysregulation can lead to abnormal cell division and contribute to the development of cancer.

Cyclin-Dependent Kinase 2 (CDK2) is a type of enzyme that plays a crucial role in the regulation of the cell cycle, which is the process by which cells grow and divide. CDK2 is activated when it binds to a regulatory subunit called a cyclin.

During the cell cycle, CDK2 helps to control the progression from the G1 phase to the S phase, where DNA replication occurs. Specifically, CDK2 phosphorylates various target proteins that are involved in the regulation of DNA replication and the initiation of mitosis, which is the process of cell division.

CDK2 activity is tightly regulated through a variety of mechanisms, including phosphorylation, dephosphorylation, and protein degradation. Dysregulation of CDK2 activity has been implicated in various human diseases, including cancer. Therefore, CDK2 is an important target for the development of therapies aimed at treating these diseases.

Cyclin T is a type of cyclin protein that is encoded by the CCNT2 gene in humans. Cyclins are a family of regulatory proteins that play a crucial role in the cell cycle, which is the series of events that cells undergo as they grow and divide. Specifically, cyclin T is a component of the CDK9/cyclin T complex, also known as positive transcription elongation factor b (P-TEFb), which plays a key role in regulating gene expression by controlling the elongation phase of RNA polymerase II-mediated transcription.

Cyclin T is expressed at various stages of the cell cycle and has been shown to interact with several other proteins involved in cell cycle regulation, including the retinoblastoma protein (pRb) and the E2F family of transcription factors. Dysregulation of cyclin T expression or activity has been implicated in several human diseases, including cancer.

Cyclin H is a type of protein that is classified as a cyclin, which is a regulatory subunit of cyclin-dependent kinases (CDKs). Specifically, Cyclin H forms a complex with CDK7 and functions as an essential component of the cell cycle transcriptional coactivator known as TFIIH.

TFIIH plays a crucial role in the initiation of transcription by RNA polymerase II and also participates in the process of DNA repair. The Cyclin H-CDK7 complex phosphorylates the carboxy-terminal domain (CTD) of the largest subunit of RNA polymerase II, which is a critical step in the transcription cycle. Additionally, Cyclin H-CDK7 also plays a role in regulating the cell cycle by controlling the activity of certain cell cycle regulators, such as E2F transcription factors.

Mutations in the gene that encodes Cyclin H have been associated with certain human diseases, including a rare inherited disorder called Cockayne syndrome, which is characterized by developmental abnormalities, neurological dysfunction, and premature aging.

The G1 phase, or Gap 1 phase, is the first phase of the cell cycle, during which the cell grows in size and synthesizes mRNA and proteins in preparation for subsequent steps leading to mitosis. During this phase, the cell also checks its growth and makes sure that it is large enough to proceed through the cell cycle. If the cell is not large enough, it will arrest in the G1 phase until it has grown sufficiently. The G1 phase is followed by the S phase, during which DNA replication occurs.

Cyclin-Dependent Kinase 4 (CDK4) is a type of enzyme, specifically a serine/threonine protein kinase, that plays a crucial role in the regulation of the cell cycle. The cell cycle is the series of events that take place in a cell leading to its division and duplication. CDK4, when activated by binding to cyclin D, helps to promote the transition from the G1 phase to the S phase of the cell cycle. This transition is a critical point in the regulation of cell growth and division, and dysregulation of this process can lead to uncontrolled cell growth and cancer. CDK4 inhibitors are used in the treatment of certain types of cancer, such as breast and lung cancer, to block the activity of CDK4 and prevent tumor cell proliferation.

CDC2 and CDC28 are members of the Serine/Threonine protein kinase family, which play crucial roles in the regulation of the cell cycle. These kinases were originally identified in yeast (CDC28) and humans (CDC2), but they are highly conserved across eukaryotes.

CDC2-CDC28 Kinases function as a part of larger complexes, often associated with cyclins, to control different phases of the cell cycle by phosphorylating specific substrates at key regulatory points. The activity of CDC2-CDC28 Kinases is tightly regulated through various mechanisms, including phosphorylation, dephosphorylation, and protein binding interactions.

During the G2 phase of the cell cycle, CDC2-CDC28 Kinases are inactivated by phosphorylation at specific residues (Tyr15 and Thr14). As the cell approaches mitosis, a family of phosphatases called Cdc25 removes these inhibitory phosphates, leading to activation of the kinase. Activated CDC2-CDC28 Kinases then initiate mitotic processes such as chromosome condensation and nuclear envelope breakdown.

In summary, CDC2-CDC28 Kinases are essential regulators of the eukaryotic cell cycle, controlling various aspects of cell division through phosphorylation of specific substrates. Their activity is tightly regulated to ensure proper progression through the cell cycle and prevent uncontrolled cell growth, which can lead to diseases such as cancer.

CDC2 protein kinase, also known as cell division cycle 2 or CDK1, is a type of enzyme that plays a crucial role in the regulation of the cell cycle. The cell cycle is the series of events that cells undergo as they grow, replicate their DNA, and divide into two daughter cells.

CDC2 protein kinase is a member of the cyclin-dependent kinase (CDK) family, which are serine/threonine protein kinases that are activated by binding to regulatory subunits called cyclins. CDC2 protein kinase is primarily associated with the regulation of the G2 phase and the entry into mitosis, the stage of the cell cycle where nuclear and cytoplasmic division occur.

CDC2 protein kinase functions by phosphorylating various target proteins, which alters their activity and contributes to the coordination of the different events that occur during the cell cycle. The activity of CDC2 protein kinase is tightly regulated through a variety of mechanisms, including phosphorylation and dephosphorylation, as well as the binding and destruction of cyclin subunits.

Dysregulation of CDC2 protein kinase has been implicated in various human diseases, including cancer, where uncontrolled cell division can lead to the formation of tumors. Therefore, understanding the regulation and function of CDC2 protein kinase is an important area of research in molecular biology and medicine.

In the context of cell biology, "S phase" refers to the part of the cell cycle during which DNA replication occurs. The "S" stands for synthesis, reflecting the active DNA synthesis that takes place during this phase. It is preceded by G1 phase (gap 1) and followed by G2 phase (gap 2), with mitosis (M phase) being the final stage of the cell cycle.

During S phase, the cell's DNA content effectively doubles as each chromosome is replicated to ensure that the two resulting daughter cells will have the same genetic material as the parent cell. This process is carefully regulated and coordinated with other events in the cell cycle to maintain genomic stability.

Retinoblastoma Protein (pRb or RB1) is a tumor suppressor protein that plays a critical role in regulating the cell cycle and preventing uncontrolled cell growth. It is encoded by the RB1 gene, located on chromosome 13. The retinoblastoma protein functions as a regulatory checkpoint in the cell cycle, preventing cells from progressing into the S phase (DNA synthesis phase) until certain conditions are met.

When pRb is in its active state, it binds to and inhibits the activity of E2F transcription factors, which promote the expression of genes required for DNA replication and cell cycle progression. Phosphorylation of pRb by cyclin-dependent kinases (CDKs) leads to the release of E2F factors, allowing them to activate their target genes and drive the cell into S phase.

Mutations in the RB1 gene can result in the production of a nonfunctional or reduced amount of pRb protein, leading to uncontrolled cell growth and an increased risk of developing retinoblastoma, a rare form of eye cancer, as well as other types of tumors.

Protein Phosphatase 2 (PP2A) is a type of serine/threonine protein phosphatase that plays a crucial role in the regulation of various cellular processes, including signal transduction, cell cycle progression, and metabolism. PP2A is a heterotrimeric enzyme composed of a catalytic subunit (C), a regulatory subunit A (A), and a variable regulatory subunit B (B). The different combinations of the B subunits confer specificity to PP2A, allowing it to regulate a diverse array of cellular targets.

PP2A is responsible for dephosphorylating many proteins that have been previously phosphorylated by protein kinases. This function is essential for maintaining the balance of phosphorylation and dephosphorylation in cells, which is necessary for proper protein function and cell signaling. Dysregulation of PP2A has been implicated in various diseases, including cancer, neurodegenerative disorders, and cardiovascular disease.

Tumor suppressor protein p53, also known as p53 or tumor protein p53, is a nuclear phosphoprotein that plays a crucial role in preventing cancer development and maintaining genomic stability. It does so by regulating the cell cycle and acting as a transcription factor for various genes involved in apoptosis (programmed cell death), DNA repair, and cell senescence (permanent cell growth arrest).

In response to cellular stress, such as DNA damage or oncogene activation, p53 becomes activated and accumulates in the nucleus. Activated p53 can then bind to specific DNA sequences and promote the transcription of target genes that help prevent the proliferation of potentially cancerous cells. These targets include genes involved in cell cycle arrest (e.g., CDKN1A/p21), apoptosis (e.g., BAX, PUMA), and DNA repair (e.g., GADD45).

Mutations in the TP53 gene, which encodes p53, are among the most common genetic alterations found in human cancers. These mutations often lead to a loss or reduction of p53's tumor suppressive functions, allowing cancer cells to proliferate uncontrollably and evade apoptosis. As a result, p53 has been referred to as "the guardian of the genome" due to its essential role in preventing tumorigenesis.

The G2 phase, also known as the "gap 2 phase," is a stage in the cell cycle that occurs after DNA replication (S phase) and before cell division (mitosis). During this phase, the cell prepares for mitosis by completing the synthesis of proteins and organelles needed for chromosome separation. The cell also checks for any errors or damage to the DNA before entering mitosis. This phase is a critical point in the cell cycle where proper regulation ensures the faithful transmission of genetic information from one generation of cells to the next. If significant DNA damage is detected during G2, the cell may undergo programmed cell death (apoptosis) instead of dividing.

Cell cycle proteins are a group of regulatory proteins that control the progression of the cell cycle, which is the series of events that take place in a eukaryotic cell leading to its division and duplication. These proteins can be classified into several categories based on their functions during different stages of the cell cycle.

The major groups of cell cycle proteins include:

1. Cyclin-dependent kinases (CDKs): CDKs are serine/threonine protein kinases that regulate key transitions in the cell cycle. They require binding to a regulatory subunit called cyclin to become active. Different CDK-cyclin complexes are activated at different stages of the cell cycle.
2. Cyclins: Cyclins are a family of regulatory proteins that bind and activate CDKs. Their levels fluctuate throughout the cell cycle, with specific cyclins expressed during particular phases. For example, cyclin D is important for the G1 to S phase transition, while cyclin B is required for the G2 to M phase transition.
3. CDK inhibitors (CKIs): CKIs are regulatory proteins that bind to and inhibit CDKs, thereby preventing their activation. CKIs can be divided into two main families: the INK4 family and the Cip/Kip family. INK4 family members specifically inhibit CDK4 and CDK6, while Cip/Kip family members inhibit a broader range of CDKs.
4. Anaphase-promoting complex/cyclosome (APC/C): APC/C is an E3 ubiquitin ligase that targets specific proteins for degradation by the 26S proteasome. During the cell cycle, APC/C regulates the metaphase to anaphase transition and the exit from mitosis by targeting securin and cyclin B for degradation.
5. Other regulatory proteins: Several other proteins play crucial roles in regulating the cell cycle, such as p53, a transcription factor that responds to DNA damage and arrests the cell cycle, and the polo-like kinases (PLKs), which are involved in various aspects of mitosis.

Overall, cell cycle proteins work together to ensure the proper progression of the cell cycle, maintain genomic stability, and prevent uncontrolled cell growth, which can lead to cancer.

Mitosis is a type of cell division in which the genetic material of a single cell, called the mother cell, is equally distributed into two identical daughter cells. It's a fundamental process that occurs in multicellular organisms for growth, maintenance, and repair, as well as in unicellular organisms for reproduction.

The process of mitosis can be broken down into several stages: prophase, prometaphase, metaphase, anaphase, and telophase. During prophase, the chromosomes condense and become visible, and the nuclear envelope breaks down. In prometaphase, the nuclear membrane is completely disassembled, and the mitotic spindle fibers attach to the chromosomes at their centromeres.

During metaphase, the chromosomes align at the metaphase plate, an imaginary line equidistant from the two spindle poles. In anaphase, sister chromatids are pulled apart by the spindle fibers and move toward opposite poles of the cell. Finally, in telophase, new nuclear envelopes form around each set of chromosomes, and the chromosomes decondense and become less visible.

Mitosis is followed by cytokinesis, a process that divides the cytoplasm of the mother cell into two separate daughter cells. The result of mitosis and cytokinesis is two genetically identical cells, each with the same number and kind of chromosomes as the original parent cell.

Cyclin-Dependent Kinase Inhibitor p27, also known as CDKN1B or p27Kip1, is a protein that regulates the cell cycle. It inhibits the activity of certain cyclin-dependent kinases (CDKs), which are enzymes that play key roles in regulating the progression of the cell cycle.

The cell cycle is a series of events that cells undergo as they grow and divide. Cyclins and CDKs help to control the different stages of the cell cycle by activating and deactivating various proteins at specific times. The p27 protein acts as a brake on the cell cycle, preventing cells from dividing too quickly or abnormally.

When p27 binds to a CDK-cyclin complex, it prevents the complex from phosphorylating its target proteins, which are necessary for the progression of the cell cycle. By inhibiting CDK activity, p27 helps to ensure that cells divide only when the proper conditions are met.

Mutations in the CDKN1B gene, which encodes p27, have been associated with several types of cancer, including breast, lung, and prostate cancer. These mutations can lead to decreased levels of p27 or impaired function, allowing cells to divide uncontrollably and form tumors.

I'm sorry for any confusion, but a specific medical definition for 'Cyclin I' could not be found. Cyclins are a family of proteins that regulate the cell cycle in cells. They are so named because their levels fluctuate or cycle during different phases of the cell cycle. However, there is no specific cyclin referred to as "Cyclin I" in current medical and scientific literature.

There is a protein called "cyclin I" found in some organisms like Drosophila melanogaster (fruit flies), but it doesn't have a well-established role or equivalent in human cell cycle regulation. Therefore, it may not be relevant to provide a medical definition for a protein that is not directly involved in human physiology or pathophysiology.

Cyclin-dependent kinase inhibitor p21, also known as CDKN1A or p21/WAF1/CIP1, is a protein that regulates the cell cycle. It inhibits the activity of cyclin-dependent kinases (CDKs), which are enzymes that play crucial roles in controlling the progression of the cell cycle.

The binding of p21 to CDKs prevents the phosphorylation and activation of downstream targets, leading to cell cycle arrest. This protein is transcriptionally activated by tumor suppressor protein p53 in response to DNA damage or other stress signals, and it functions as an important mediator of p53-dependent growth arrest.

By inhibiting CDKs, p21 helps to ensure that cells do not proceed through the cell cycle until damaged DNA has been repaired, thereby preventing the propagation of potentially harmful mutations. Additionally, p21 has been implicated in other cellular processes such as apoptosis, differentiation, and senescence. Dysregulation of p21 has been associated with various human diseases, including cancer.

Phosphorylation is the process of adding a phosphate group (a molecule consisting of one phosphorus atom and four oxygen atoms) to a protein or other organic molecule, which is usually done by enzymes called kinases. This post-translational modification can change the function, localization, or activity of the target molecule, playing a crucial role in various cellular processes such as signal transduction, metabolism, and regulation of gene expression. Phosphorylation is reversible, and the removal of the phosphate group is facilitated by enzymes called phosphatases.

A cell line that is derived from tumor cells and has been adapted to grow in culture. These cell lines are often used in research to study the characteristics of cancer cells, including their growth patterns, genetic changes, and responses to various treatments. They can be established from many different types of tumors, such as carcinomas, sarcomas, and leukemias. Once established, these cell lines can be grown and maintained indefinitely in the laboratory, allowing researchers to conduct experiments and studies that would not be feasible using primary tumor cells. It is important to note that tumor cell lines may not always accurately represent the behavior of the original tumor, as they can undergo genetic changes during their time in culture.

Cell division is the process by which a single eukaryotic cell (a cell with a true nucleus) divides into two identical daughter cells. This complex process involves several stages, including replication of DNA, separation of chromosomes, and division of the cytoplasm. There are two main types of cell division: mitosis and meiosis.

Mitosis is the type of cell division that results in two genetically identical daughter cells. It is a fundamental process for growth, development, and tissue repair in multicellular organisms. The stages of mitosis include prophase, prometaphase, metaphase, anaphase, and telophase, followed by cytokinesis, which divides the cytoplasm.

Meiosis, on the other hand, is a type of cell division that occurs in the gonads (ovaries and testes) during the production of gametes (sex cells). Meiosis results in four genetically unique daughter cells, each with half the number of chromosomes as the parent cell. This process is essential for sexual reproduction and genetic diversity. The stages of meiosis include meiosis I and meiosis II, which are further divided into prophase, prometaphase, metaphase, anaphase, and telophase.

In summary, cell division is the process by which a single cell divides into two daughter cells, either through mitosis or meiosis. This process is critical for growth, development, tissue repair, and sexual reproduction in multicellular organisms.

NIH 3T3 cells are a type of mouse fibroblast cell line that was developed by the National Institutes of Health (NIH). The "3T3" designation refers to the fact that these cells were derived from embryonic Swiss mouse tissue and were able to be passaged (i.e., subcultured) more than three times in tissue culture.

NIH 3T3 cells are widely used in scientific research, particularly in studies involving cell growth and differentiation, signal transduction, and gene expression. They have also been used as a model system for studying the effects of various chemicals and drugs on cell behavior. NIH 3T3 cells are known to be relatively easy to culture and maintain, and they have a stable, flat morphology that makes them well-suited for use in microscopy studies.

It is important to note that, as with any cell line, it is essential to verify the identity and authenticity of NIH 3T3 cells before using them in research, as contamination or misidentification can lead to erroneous results.

Oncogene proteins are derived from oncogenes, which are genes that have the potential to cause cancer. Normally, these genes help regulate cell growth and division, but when they become altered or mutated, they can become overactive and lead to uncontrolled cell growth and division, which is a hallmark of cancer. Oncogene proteins can contribute to tumor formation and progression by promoting processes such as cell proliferation, survival, angiogenesis, and metastasis. Examples of oncogene proteins include HER2/neu, EGFR, and BCR-ABL.

BCL-1 (B-cell leukemia/lymphoma 1) is not a gene itself but rather a chromosomal translocation that results in the formation of an abnormal fusion gene. The BCL-1 translocation, also known as t(14;18)(q32;q21), is most commonly found in follicular lymphoma, a type of slow-growing non-Hodgkin lymphoma.

The BCL-1 translocation involves the juxtaposition of the BCL-2 gene, which is located on chromosome 18, with the IGH (immunoglobulin heavy chain) gene, which is located on chromosome 14. This translocation results in the overexpression of the BCL-2 protein, which inhibits apoptosis or programmed cell death. The overexpression of BCL-2 leads to the accumulation of cancer cells and contributes to the development and progression of follicular lymphoma.

It is important to note that while BCL-1 is a chromosomal translocation, it can also refer to the protein encoded by the BCL-2 gene when it is overexpressed due to the t(14;18) translocation. In this context, BCL-1 is considered a proto-oncogene because its overexpression promotes cancer development and progression.

Interleukin-12 (IL-12) receptor beta 2 subunit is a protein that forms part of the IL-12 receptor complex, which is found on the surface of certain immune cells, such as T cells and natural killer cells. The IL-12 receptor is a heterodimeric receptor composed of two subunits, IL-12Rβ1 and IL-12Rβ2.

IL-12 is a cytokine that plays a critical role in the differentiation of T cells into Th1 cells, which are important for cell-mediated immunity against intracellular pathogens such as viruses and bacteria. The binding of IL-12 to its receptor leads to the activation of several signaling pathways that result in the production of interferon-gamma (IFN-γ) and the differentiation of Th1 cells.

The IL-12Rβ2 subunit is essential for the formation of a high-affinity IL-12 receptor complex, as it has a higher binding affinity for IL-12 than the IL-12Rβ1 subunit. The expression of IL-12Rβ2 is tightly regulated and is primarily found on activated T cells and natural killer cells. Mutations in the gene encoding the IL-12Rβ2 subunit have been associated with immunodeficiency disorders, including Mendelian susceptibility to mycobacterial diseases (MSMD).

Proto-oncogene proteins, such as c-MDM2, are normal cellular proteins that play crucial roles in regulating various cellular processes, including cell growth, differentiation, and apoptosis (programmed cell death). When these genes undergo mutations or are overexpressed, they can become oncogenes, which contribute to the development of cancer.

The c-MDM2 protein is a key regulator of the cell cycle and is involved in the negative regulation of the tumor suppressor protein p53. Under normal conditions, p53 helps prevent the formation of tumors by inducing cell cycle arrest or apoptosis in response to DNA damage or other stress signals. However, when c-MDM2 is overexpressed or mutated, it can bind and inhibit p53, leading to uncontrolled cell growth and increased risk of cancer development.

In summary, proto-oncogene proteins like c-MDM2 are important regulators of normal cellular processes, but when they become dysregulated through mutations or overexpression, they can contribute to the formation of tumors and cancer progression.

Cell proliferation is the process by which cells increase in number, typically through the process of cell division. In the context of biology and medicine, it refers to the reproduction of cells that makes up living tissue, allowing growth, maintenance, and repair. It involves several stages including the transition from a phase of quiescence (G0 phase) to an active phase (G1 phase), DNA replication in the S phase, and mitosis or M phase, where the cell divides into two daughter cells.

Abnormal or uncontrolled cell proliferation is a characteristic feature of many diseases, including cancer, where deregulated cell cycle control leads to excessive and unregulated growth of cells, forming tumors that can invade surrounding tissues and metastasize to distant sites in the body.

The cell nucleus is a membrane-bound organelle found in the eukaryotic cells (cells with a true nucleus). It contains most of the cell's genetic material, organized as DNA molecules in complex with proteins, RNA molecules, and histones to form chromosomes.

The primary function of the cell nucleus is to regulate and control the activities of the cell, including growth, metabolism, protein synthesis, and reproduction. It also plays a crucial role in the process of mitosis (cell division) by separating and protecting the genetic material during this process. The nuclear membrane, or nuclear envelope, surrounding the nucleus is composed of two lipid bilayers with numerous pores that allow for the selective transport of molecules between the nucleoplasm (nucleus interior) and the cytoplasm (cell exterior).

The cell nucleus is a vital structure in eukaryotic cells, and its dysfunction can lead to various diseases, including cancer and genetic disorders.

Protein-Serine-Threonine Kinases (PSTKs) are a type of protein kinase that catalyzes the transfer of a phosphate group from ATP to the hydroxyl side chains of serine or threonine residues on target proteins. This phosphorylation process plays a crucial role in various cellular signaling pathways, including regulation of metabolism, gene expression, cell cycle progression, and apoptosis. PSTKs are involved in many physiological and pathological processes, and their dysregulation has been implicated in several diseases, such as cancer, diabetes, and neurodegenerative disorders.

Cyclin-Dependent Kinase 6 (CDK6) is a type of enzyme known as a protein kinase, which adds phosphate groups to other proteins in the cell. CDK6 is primarily involved in regulating the cell cycle, the process by which cells divide and grow.

CDK6 functions by binding to cyclin proteins, forming active complexes that help drive the progression of the cell cycle from one phase to the next. Specifically, CDK6 plays a crucial role in the transition from the G1 phase to the S phase of the cell cycle, where DNA replication occurs.

CDK6 activity is tightly regulated by various mechanisms, including phosphorylation and dephosphorylation, as well as by binding to inhibitory proteins such as p16INK4a and p21CIP1. Dysregulation of CDK6 has been implicated in the development of several types of cancer, making it a potential target for cancer therapy.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

Down-regulation is a process that occurs in response to various stimuli, where the number or sensitivity of cell surface receptors or the expression of specific genes is decreased. This process helps maintain homeostasis within cells and tissues by reducing the ability of cells to respond to certain signals or molecules.

In the context of cell surface receptors, down-regulation can occur through several mechanisms:

1. Receptor internalization: After binding to their ligands, receptors can be internalized into the cell through endocytosis. Once inside the cell, these receptors may be degraded or recycled back to the cell surface in smaller numbers.
2. Reduced receptor synthesis: Down-regulation can also occur at the transcriptional level, where the expression of genes encoding for specific receptors is decreased, leading to fewer receptors being produced.
3. Receptor desensitization: Prolonged exposure to a ligand can lead to a decrease in receptor sensitivity or affinity, making it more difficult for the cell to respond to the signal.

In the context of gene expression, down-regulation refers to the decreased transcription and/or stability of specific mRNAs, leading to reduced protein levels. This process can be induced by various factors, including microRNA (miRNA)-mediated regulation, histone modification, or DNA methylation.

Down-regulation is an essential mechanism in many physiological processes and can also contribute to the development of several diseases, such as cancer and neurodegenerative disorders.

Transfection is a term used in molecular biology that refers to the process of deliberately introducing foreign genetic material (DNA, RNA or artificial gene constructs) into cells. This is typically done using chemical or physical methods, such as lipofection or electroporation. Transfection is widely used in research and medical settings for various purposes, including studying gene function, producing proteins, developing gene therapies, and creating genetically modified organisms. It's important to note that transfection is different from transduction, which is the process of introducing genetic material into cells using viruses as vectors.

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

Adenocarcinoma, papillary is a type of cancer that begins in the glandular cells and grows in a finger-like projection (called a papilla). This type of cancer can occur in various organs, including the lungs, pancreas, thyroid, and female reproductive system. The prognosis and treatment options for papillary adenocarcinoma depend on several factors, such as the location and stage of the tumor, as well as the patient's overall health. It is important to consult with a healthcare professional for an accurate diagnosis and personalized treatment plan.

Protein binding, in the context of medical and biological sciences, refers to the interaction between a protein and another molecule (known as the ligand) that results in a stable complex. This process is often reversible and can be influenced by various factors such as pH, temperature, and concentration of the involved molecules.

In clinical chemistry, protein binding is particularly important when it comes to drugs, as many of them bind to proteins (especially albumin) in the bloodstream. The degree of protein binding can affect a drug's distribution, metabolism, and excretion, which in turn influence its therapeutic effectiveness and potential side effects.

Protein-bound drugs may be less available for interaction with their target tissues, as only the unbound or "free" fraction of the drug is active. Therefore, understanding protein binding can help optimize dosing regimens and minimize adverse reactions.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

The proteasome endopeptidase complex is a large protein complex found in the cells of eukaryotic organisms, as well as in archaea and some bacteria. It plays a crucial role in the degradation of damaged or unneeded proteins through a process called proteolysis. The proteasome complex contains multiple subunits, including both regulatory and catalytic particles.

The catalytic core of the proteasome is composed of four stacked rings, each containing seven subunits, forming a structure known as the 20S core particle. Three of these rings are made up of beta-subunits that contain the proteolytic active sites, while the fourth ring consists of alpha-subunits that control access to the interior of the complex.

The regulatory particles, called 19S or 11S regulators, cap the ends of the 20S core particle and are responsible for recognizing, unfolding, and translocating targeted proteins into the catalytic chamber. The proteasome endopeptidase complex can cleave peptide bonds in various ways, including hydrolysis of ubiquitinated proteins, which is an essential mechanism for maintaining protein quality control and regulating numerous cellular processes, such as cell cycle progression, signal transduction, and stress response.

In summary, the proteasome endopeptidase complex is a crucial intracellular machinery responsible for targeted protein degradation through proteolysis, contributing to various essential regulatory functions in cells.

Neoplastic gene expression regulation refers to the processes that control the production of proteins and other molecules from genes in neoplastic cells, or cells that are part of a tumor or cancer. In a normal cell, gene expression is tightly regulated to ensure that the right genes are turned on or off at the right time. However, in cancer cells, this regulation can be disrupted, leading to the overexpression or underexpression of certain genes.

Neoplastic gene expression regulation can be affected by a variety of factors, including genetic mutations, epigenetic changes, and signals from the tumor microenvironment. These changes can lead to the activation of oncogenes (genes that promote cancer growth and development) or the inactivation of tumor suppressor genes (genes that prevent cancer).

Understanding neoplastic gene expression regulation is important for developing new therapies for cancer, as targeting specific genes or pathways involved in this process can help to inhibit cancer growth and progression.

S-phase kinase-associated proteins (Skp2) are a group of proteins that are associated with the S-phase kinase, which is a type of enzyme that helps to regulate the cell cycle. Specifically, Skp2 is involved in the ubiquitination and degradation of certain proteins that play a role in controlling the progression of the cell cycle.

Skp2 is a member of the F-box protein family, which are components of the Skp1-Cul1-F-box (SCF) complex, a type of E3 ubiquitin ligase. The SCF complex recognizes and binds to specific proteins, tagging them for ubiquitination and subsequent degradation by the proteasome.

One of the key targets of Skp2 is the tumor suppressor protein p27, which inhibits the activity of cyclin-dependent kinases (CDKs) and helps to regulate the transition from the G1 phase to the S phase of the cell cycle. By targeting p27 for degradation, Skp2 promotes the progression of the cell cycle and has been implicated in the development of various types of cancer.

Overall, Skp2 plays a critical role in regulating the cell cycle and has important implications for the development and treatment of various diseases, including cancer.

'Tumor cells, cultured' refers to the process of removing cancerous cells from a tumor and growing them in controlled laboratory conditions. This is typically done by isolating the tumor cells from a patient's tissue sample, then placing them in a nutrient-rich environment that promotes their growth and multiplication.

The resulting cultured tumor cells can be used for various research purposes, including the study of cancer biology, drug development, and toxicity testing. They provide a valuable tool for researchers to better understand the behavior and characteristics of cancer cells outside of the human body, which can lead to the development of more effective cancer treatments.

It is important to note that cultured tumor cells may not always behave exactly the same way as they do in the human body, so findings from cell culture studies must be validated through further research, such as animal models or clinical trials.

Proto-oncogene proteins are normal cellular proteins that play crucial roles in various cellular processes, such as signal transduction, cell cycle regulation, and apoptosis (programmed cell death). They are involved in the regulation of cell growth, differentiation, and survival under physiological conditions.

When proto-oncogene proteins undergo mutations or aberrations in their expression levels, they can transform into oncogenic forms, leading to uncontrolled cell growth and division. These altered proteins are then referred to as oncogene products or oncoproteins. Oncogenic mutations can occur due to various factors, including genetic predisposition, environmental exposures, and aging.

Examples of proto-oncogene proteins include:

1. Ras proteins: Involved in signal transduction pathways that regulate cell growth and differentiation. Activating mutations in Ras genes are found in various human cancers.
2. Myc proteins: Regulate gene expression related to cell cycle progression, apoptosis, and metabolism. Overexpression of Myc proteins is associated with several types of cancer.
3. EGFR (Epidermal Growth Factor Receptor): A transmembrane receptor tyrosine kinase that regulates cell proliferation, survival, and differentiation. Mutations or overexpression of EGFR are linked to various malignancies, such as lung cancer and glioblastoma.
4. Src family kinases: Intracellular tyrosine kinases that regulate signal transduction pathways involved in cell proliferation, survival, and migration. Dysregulation of Src family kinases is implicated in several types of cancer.
5. Abl kinases: Cytoplasmic tyrosine kinases that regulate various cellular processes, including cell growth, differentiation, and stress responses. Aberrant activation of Abl kinases, as seen in chronic myelogenous leukemia (CML), leads to uncontrolled cell proliferation.

Understanding the roles of proto-oncogene proteins and their dysregulation in cancer development is essential for developing targeted cancer therapies that aim to inhibit or modulate these aberrant signaling pathways.

DNA damage refers to any alteration in the structure or composition of deoxyribonucleic acid (DNA), which is the genetic material present in cells. DNA damage can result from various internal and external factors, including environmental exposures such as ultraviolet radiation, tobacco smoke, and certain chemicals, as well as normal cellular processes such as replication and oxidative metabolism.

Examples of DNA damage include base modifications, base deletions or insertions, single-strand breaks, double-strand breaks, and crosslinks between the two strands of the DNA helix. These types of damage can lead to mutations, genomic instability, and chromosomal aberrations, which can contribute to the development of diseases such as cancer, neurodegenerative disorders, and aging-related conditions.

The body has several mechanisms for repairing DNA damage, including base excision repair, nucleotide excision repair, mismatch repair, and double-strand break repair. However, if the damage is too extensive or the repair mechanisms are impaired, the cell may undergo apoptosis (programmed cell death) to prevent the propagation of potentially harmful mutations.

3T3 cells are a type of cell line that is commonly used in scientific research. The name "3T3" is derived from the fact that these cells were developed by treating mouse embryo cells with a chemical called trypsin and then culturing them in a flask at a temperature of 37 degrees Celsius.

Specifically, 3T3 cells are a type of fibroblast, which is a type of cell that is responsible for producing connective tissue in the body. They are often used in studies involving cell growth and proliferation, as well as in toxicity tests and drug screening assays.

One particularly well-known use of 3T3 cells is in the 3T3-L1 cell line, which is a subtype of 3T3 cells that can be differentiated into adipocytes (fat cells) under certain conditions. These cells are often used in studies of adipose tissue biology and obesity.

It's important to note that because 3T3 cells are a type of immortalized cell line, they do not always behave exactly the same way as primary cells (cells that are taken directly from a living organism). As such, researchers must be careful when interpreting results obtained using 3T3 cells and consider any potential limitations or artifacts that may arise due to their use.

An amino acid sequence is the specific order of amino acids in a protein or peptide molecule, formed by the linking of the amino group (-NH2) of one amino acid to the carboxyl group (-COOH) of another amino acid through a peptide bond. The sequence is determined by the genetic code and is unique to each type of protein or peptide. It plays a crucial role in determining the three-dimensional structure and function of proteins.

Phosphoprotein phosphatases (PPPs) are a family of enzymes that play a crucial role in the regulation of various cellular processes by removing phosphate groups from serine, threonine, and tyrosine residues on proteins. Phosphorylation is a post-translational modification that regulates protein function, localization, and stability, and dephosphorylation by PPPs is essential for maintaining the balance of this regulation.

The PPP family includes several subfamilies, such as PP1, PP2A, PP2B (also known as calcineurin), PP4, PP5, and PP6. Each subfamily has distinct substrate specificities and regulatory mechanisms. For example, PP1 and PP2A are involved in the regulation of metabolism, signal transduction, and cell cycle progression, while PP2B is involved in immune response and calcium signaling.

Dysregulation of PPPs has been implicated in various diseases, including cancer, neurodegenerative disorders, and cardiovascular disease. Therefore, understanding the function and regulation of PPPs is important for developing therapeutic strategies to target these diseases.

Nuclear proteins are a category of proteins that are primarily found in the nucleus of a eukaryotic cell. They play crucial roles in various nuclear functions, such as DNA replication, transcription, repair, and RNA processing. This group includes structural proteins like lamins, which form the nuclear lamina, and regulatory proteins, such as histones and transcription factors, that are involved in gene expression. Nuclear localization signals (NLS) often help target these proteins to the nucleus by interacting with importin proteins during active transport across the nuclear membrane.

Recombinant fusion proteins are artificially created biomolecules that combine the functional domains or properties of two or more different proteins into a single protein entity. They are generated through recombinant DNA technology, where the genes encoding the desired protein domains are linked together and expressed as a single, chimeric gene in a host organism, such as bacteria, yeast, or mammalian cells.

The resulting fusion protein retains the functional properties of its individual constituent proteins, allowing for novel applications in research, diagnostics, and therapeutics. For instance, recombinant fusion proteins can be designed to enhance protein stability, solubility, or immunogenicity, making them valuable tools for studying protein-protein interactions, developing targeted therapies, or generating vaccines against infectious diseases or cancer.

Examples of recombinant fusion proteins include:

1. Etaglunatide (ABT-523): A soluble Fc fusion protein that combines the heavy chain fragment crystallizable region (Fc) of an immunoglobulin with the extracellular domain of the human interleukin-6 receptor (IL-6R). This fusion protein functions as a decoy receptor, neutralizing IL-6 and its downstream signaling pathways in rheumatoid arthritis.
2. Etanercept (Enbrel): A soluble TNF receptor p75 Fc fusion protein that binds to tumor necrosis factor-alpha (TNF-α) and inhibits its proinflammatory activity, making it a valuable therapeutic option for treating autoimmune diseases like rheumatoid arthritis, ankylosing spondylitis, and psoriasis.
3. Abatacept (Orencia): A fusion protein consisting of the extracellular domain of cytotoxic T-lymphocyte antigen 4 (CTLA-4) linked to the Fc region of an immunoglobulin, which downregulates T-cell activation and proliferation in autoimmune diseases like rheumatoid arthritis.
4. Belimumab (Benlysta): A monoclonal antibody that targets B-lymphocyte stimulator (BLyS) protein, preventing its interaction with the B-cell surface receptor and inhibiting B-cell activation in systemic lupus erythematosus (SLE).
5. Romiplostim (Nplate): A fusion protein consisting of a thrombopoietin receptor agonist peptide linked to an immunoglobulin Fc region, which stimulates platelet production in patients with chronic immune thrombocytopenia (ITP).
6. Darbepoetin alfa (Aranesp): A hyperglycosylated erythropoiesis-stimulating protein that functions as a longer-acting form of recombinant human erythropoietin, used to treat anemia in patients with chronic kidney disease or cancer.
7. Palivizumab (Synagis): A monoclonal antibody directed against the F protein of respiratory syncytial virus (RSV), which prevents RSV infection and is administered prophylactically to high-risk infants during the RSV season.
8. Ranibizumab (Lucentis): A recombinant humanized monoclonal antibody fragment that binds and inhibits vascular endothelial growth factor A (VEGF-A), used in the treatment of age-related macular degeneration, diabetic retinopathy, and other ocular disorders.
9. Cetuximab (Erbitux): A chimeric monoclonal antibody that binds to epidermal growth factor receptor (EGFR), used in the treatment of colorectal cancer and head and neck squamous cell carcinoma.
10. Adalimumab (Humira): A fully humanized monoclonal antibody that targets tumor necrosis factor-alpha (TNF-α), used in the treatment of various inflammatory diseases, including rheumatoid arthritis, psoriasis, and Crohn's disease.
11. Bevacizumab (Avastin): A recombinant humanized monoclonal antibody that binds to VEGF-A, used in the treatment of various cancers, including colorectal, lung, breast, and kidney cancer.
12. Trastuzumab (Herceptin): A humanized monoclonal antibody that targets HER2/neu receptor, used in the treatment of breast cancer.
13. Rituximab (Rituxan): A chimeric monoclonal antibody that binds to CD20 antigen on B cells, used in the treatment of non-Hodgkin's lymphoma and rheumatoid arthritis.
14. Palivizumab (Synagis): A humanized monoclonal antibody that binds to the F protein of respiratory syncytial virus, used in the prevention of respiratory syncytial virus infection in high-risk infants.
15. Infliximab (Remicade): A chimeric monoclonal antibody that targets TNF-α, used in the treatment of various inflammatory diseases, including Crohn's disease, ulcerative colitis, rheumatoid arthritis, and ankylosing spondylitis.
16. Natalizumab (Tysabri): A humanized monoclonal antibody that binds to α4β1 integrin, used in the treatment of multiple sclerosis and Crohn's disease.
17. Adalimumab (Humira): A fully human monoclonal antibody that targets TNF-α, used in the treatment of various inflammatory diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn's disease, and ulcerative colitis.
18. Golimumab (Simponi): A fully human monoclonal antibody that targets TNF-α, used in the treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and ulcerative colitis.
19. Certolizumab pegol (Cimzia): A PEGylated Fab' fragment of a humanized monoclonal antibody that targets TNF-α, used in the treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease.
20. Ustekinumab (Stelara): A fully human monoclonal antibody that targets IL-12 and IL-23, used in the treatment of psoriasis, psoriatic arthritis, and Crohn's disease.
21. Secukinumab (Cosentyx): A fully human monoclonal antibody that targets IL-17A, used in the treatment of psoriasis, psoriatic arthritis, and ankylosing spondylitis.
22. Ixekizumab (Taltz): A fully human monoclonal antibody that targets IL-17A, used in the treatment of psoriasis and psoriatic arthritis.
23. Brodalumab (Siliq): A fully human monoclonal antibody that targets IL-17 receptor A, used in the treatment of psoriasis.
24. Sarilumab (Kevzara): A fully human monoclonal antibody that targets the IL-6 receptor, used in the treatment of rheumatoid arthritis.
25. Tocilizumab (Actemra): A humanized monoclonal antibody that targets the IL-6 receptor, used in the treatment of rheumatoid arthritis, systemic juvenile idiopathic arthritis, polyarticular juvenile idiopathic arthritis, giant cell arteritis, and chimeric antigen receptor T-cell-induced cytokine release syndrome.
26. Siltuximab (Sylvant): A chimeric monoclonal antibody that targets IL-6, used in the treatment of multicentric Castleman disease.
27. Satralizumab (Enspryng): A humanized monoclonal antibody that targets IL-6 receptor alpha, used in the treatment of neuromyelitis optica spectrum disorder.
28. Sirukumab (Plivensia): A human monoclonal antibody that targets IL-6, used in the treatment

A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.

Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).

A kinase anchor protein (AKAP) is a type of scaffolding protein that plays a role in organizing and targeting various signaling molecules within cells. AKAPs are so named because they can bind to and anchor protein kinases, enzymes that add phosphate groups to other proteins, thereby modulating their activity. This allows for the localized regulation of signaling pathways and helps ensure that specific cellular responses occur in the correct location and at the right time. AKAPs can also bind to other signaling molecules, such as phosphatases, ion channels, and second messenger systems, forming large complexes that facilitate efficient communication between different parts of the cell.

There are many different AKAPs identified in various organisms, and they play crucial roles in a wide range of cellular processes, including cell division, signal transduction, and gene expression. Mutations or dysregulation of AKAPs have been implicated in several diseases, including cancer, cardiovascular disease, and neurological disorders. Therefore, understanding the structure, function, and regulation of AKAPs is an important area of research with potential therapeutic implications.

'Gene expression regulation' refers to the processes that control whether, when, and where a particular gene is expressed, meaning the production of a specific protein or functional RNA encoded by that gene. This complex mechanism can be influenced by various factors such as transcription factors, chromatin remodeling, DNA methylation, non-coding RNAs, and post-transcriptional modifications, among others. Proper regulation of gene expression is crucial for normal cellular function, development, and maintaining homeostasis in living organisms. Dysregulation of gene expression can lead to various diseases, including cancer and genetic disorders.

Tumor suppressor proteins are a type of regulatory protein that helps control the cell cycle and prevent cells from dividing and growing in an uncontrolled manner. They work to inhibit tumor growth by preventing the formation of tumors or slowing down their progression. These proteins can repair damaged DNA, regulate gene expression, and initiate programmed cell death (apoptosis) if the damage is too severe for repair.

Mutations in tumor suppressor genes, which provide the code for these proteins, can lead to a decrease or loss of function in the resulting protein. This can result in uncontrolled cell growth and division, leading to the formation of tumors and cancer. Examples of tumor suppressor proteins include p53, Rb (retinoblastoma), and BRCA1/2.

Detergents are cleaning agents that are often used to remove dirt, grease, and stains from various surfaces. They contain one or more surfactants, which are compounds that lower the surface tension between two substances, such as water and oil, allowing them to mix more easily. This makes it possible for detergents to lift and suspend dirt particles in water so they can be rinsed away.

Detergents may also contain other ingredients, such as builders, which help to enhance the cleaning power of the surfactants by softening hard water or removing mineral deposits. Some detergents may also include fragrances, colorants, and other additives to improve their appearance or performance.

In a medical context, detergents are sometimes used as disinfectants or antiseptics, as they can help to kill bacteria, viruses, and other microorganisms on surfaces. However, it is important to note that not all detergents are effective against all types of microorganisms, and some may even be toxic or harmful if used improperly.

It is always important to follow the manufacturer's instructions when using any cleaning product, including detergents, to ensure that they are used safely and effectively.

Transcriptional activation is the process by which a cell increases the rate of transcription of specific genes from DNA to RNA. This process is tightly regulated and plays a crucial role in various biological processes, including development, differentiation, and response to environmental stimuli.

Transcriptional activation occurs when transcription factors (proteins that bind to specific DNA sequences) interact with the promoter region of a gene and recruit co-activator proteins. These co-activators help to remodel the chromatin structure around the gene, making it more accessible for the transcription machinery to bind and initiate transcription.

Transcriptional activation can be regulated at multiple levels, including the availability and activity of transcription factors, the modification of histone proteins, and the recruitment of co-activators or co-repressors. Dysregulation of transcriptional activation has been implicated in various diseases, including cancer and genetic disorders.

Transcription factors are proteins that play a crucial role in regulating gene expression by controlling the transcription of DNA to messenger RNA (mRNA). They function by binding to specific DNA sequences, known as response elements, located in the promoter region or enhancer regions of target genes. This binding can either activate or repress the initiation of transcription, depending on the properties and interactions of the particular transcription factor. Transcription factors often act as part of a complex network of regulatory proteins that determine the precise spatiotemporal patterns of gene expression during development, differentiation, and homeostasis in an organism.

Up-regulation is a term used in molecular biology and medicine to describe an increase in the expression or activity of a gene, protein, or receptor in response to a stimulus. This can occur through various mechanisms such as increased transcription, translation, or reduced degradation of the molecule. Up-regulation can have important functional consequences, for example, enhancing the sensitivity or response of a cell to a hormone, neurotransmitter, or drug. It is a normal physiological process that can also be induced by disease or pharmacological interventions.

Fibroblasts are specialized cells that play a critical role in the body's immune response and wound healing process. They are responsible for producing and maintaining the extracellular matrix (ECM), which is the non-cellular component present within all tissues and organs, providing structural support and biochemical signals for surrounding cells.

Fibroblasts produce various ECM proteins such as collagens, elastin, fibronectin, and laminins, forming a complex network of fibers that give tissues their strength and flexibility. They also help in the regulation of tissue homeostasis by controlling the turnover of ECM components through the process of remodeling.

In response to injury or infection, fibroblasts become activated and start to proliferate rapidly, migrating towards the site of damage. Here, they participate in the inflammatory response, releasing cytokines and chemokines that attract immune cells to the area. Additionally, they deposit new ECM components to help repair the damaged tissue and restore its functionality.

Dysregulation of fibroblast activity has been implicated in several pathological conditions, including fibrosis (excessive scarring), cancer (where they can contribute to tumor growth and progression), and autoimmune diseases (such as rheumatoid arthritis).

Enzyme inhibitors are substances that bind to an enzyme and decrease its activity, preventing it from catalyzing a chemical reaction in the body. They can work by several mechanisms, including blocking the active site where the substrate binds, or binding to another site on the enzyme to change its shape and prevent substrate binding. Enzyme inhibitors are often used as drugs to treat various medical conditions, such as high blood pressure, abnormal heart rhythms, and bacterial infections. They can also be found naturally in some foods and plants, and can be used in research to understand enzyme function and regulation.

Retroviridae is a family of viruses that includes human immunodeficiency virus (HIV) and other viruses that primarily use RNA as their genetic material. The name "retrovirus" comes from the fact that these viruses reverse transcribe their RNA genome into DNA, which then becomes integrated into the host cell's genome. This is a unique characteristic of retroviruses, as most other viruses use DNA as their genetic material.

Retroviruses can cause a variety of diseases in animals and humans, including cancer, neurological disorders, and immunodeficiency syndromes like AIDS. They have a lipid membrane envelope that contains glycoprotein spikes, which allow them to attach to and enter host cells. Once inside the host cell, the viral RNA is reverse transcribed into DNA by the enzyme reverse transcriptase, which is then integrated into the host genome by the enzyme integrase.

Retroviruses can remain dormant in the host genome for extended periods of time, and may be reactivated under certain conditions to produce new viral particles. This ability to integrate into the host genome has also made retroviruses useful tools in molecular biology, where they are used as vectors for gene therapy and other genetic manipulations.

HeLa cells are a type of immortalized cell line used in scientific research. They are derived from a cancer that developed in the cervical tissue of Henrietta Lacks, an African-American woman, in 1951. After her death, cells taken from her tumor were found to be capable of continuous division and growth in a laboratory setting, making them an invaluable resource for medical research.

HeLa cells have been used in a wide range of scientific studies, including research on cancer, viruses, genetics, and drug development. They were the first human cell line to be successfully cloned and are able to grow rapidly in culture, doubling their population every 20-24 hours. This has made them an essential tool for many areas of biomedical research.

It is important to note that while HeLa cells have been instrumental in numerous scientific breakthroughs, the story of their origin raises ethical questions about informed consent and the use of human tissue in research.

... D / CDK4, Cyclin D / CDK6, and Cyclin E / CDK2 - regulates transition from G1 to S phase. G2/M cyclins - essential for ... The rise in presence of G1/S cyclins is paralleled by a rise in S cyclins. G1 cyclins do not behave like the other cyclins, in ... G1 cyclins, G1/S cyclins, S cyclins, and M cyclins. This division is useful when talking about most cell cycles, but it is not ... Note that the cyclins are now classified according to their conserved cyclin box structure, and not all these cyclins alter in ...
Cyclins function as regulators of CDK kinases. Different cyclins exhibit distinct expression and degradation patterns which ... Cyclin-T2 is a protein that in humans is encoded by the CCNT2 gene. The protein encoded by this gene belongs to the highly ... This cyclin and its kinase partner CDK9 were found to be subunits of the transcription elongation factor p-TEFb. The p-TEFb ... "Entrez Gene: CCNT2 cyclin T2". Simone C, Bagella L, Bellan C, Giordano A (Jun 2002). "Physical interaction between pRb and cdk9 ...
Cyclin-O is a protein that in humans is encoded by the CCNO gene. Cyclin O has been shown to interact with RPA2 and PCNA. ... "Entrez Gene: CCNO cyclin O". Otterlei M, Warbrick E, Nagelhus TA, Haug T, Slupphaug G, Akbari M, Aas PA, Steinsbekk K, Bakke O ... Hirst R, Gosden R, Miller D (June 2006). "The cyclin-like uracil DNA glycosylase (UDG) of murine oocytes and its relationship ... Muller SJ, Caradonna S (January 1993). "Cell cycle regulation of a human cyclin-like gene encoding uracil-DNA glycosylase". The ...
Cyclins function as activating subunits of enzymatic complex together with cyclin-dependent kinases (CDKs). Different cyclins ... Cyclin-A1 interacts with: CDC20, Cyclin-dependent kinase 2, E2F1, GNB2L1, GPS2, MYBL2, and Retinoblastoma protein. GRCh38: ... "Cyclin A1 directly interacts with B-myb and cyclin A1/cdk2 phosphorylate B-myb at functionally important serine and threonine ... "Cyclin A1 directly interacts with B-myb and cyclin A1/cdk2 phosphorylate B-myb at functionally important serine and threonine ...
... is a member of the cyclin family, specifically the B-type cyclins. The B-type cyclins, B1 and B2, associate with ... Cyclin B1 co-localizes with microtubules, whereas cyclin B2 is primarily associated with the Golgi region. Cyclin B2 also binds ... Cyclin B2 has been shown to interact with TGF beta receptor 2. Cyclin B GRCh38: Ensembl release 89: ENSG00000157456 - Ensembl, ... "Cyclin B2-null mice develop normally and are fertile whereas cyclin B1-null mice die in utero". Proc. Natl. Acad. Sci. U.S.A. ...
... is a member of the cyclin family. Cyclin B is a mitotic cyclin. The amount of cyclin B (which binds to Cdk1) and the ... Because cyclin B is necessary for cells to enter mitosis and therefore necessary for cell division, cyclin B levels are often ... The fact that cyclin B is often disregulated in cancer cells makes cyclin B an attractive biomarker. Many studies have been ... Cyclin+B at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Drosophila Cyclin B - The Interactive Fly ( ...
"Entrez Gene: CCNE1 cyclin E1". Shanahan F, Seghezzi W, Parry D, Mahony D, Lees E (February 1999). "Cyclin E associates with ... Mumberg D, Wick M, Bürger C, Haas K, Funk M, Müller R (1997). "Cyclin ET, a new splice variant of human cyclin E with a unique ... Cyclin E1 has been shown to interact with: CDC25A, CDKN1B, CUL3 Cdk1, Cyclin-dependent kinase 2, HERC5, P21, Retinoblastoma- ... Lew DJ, Dulić V, Reed SI (October 1991). "Isolation of three novel human cyclins by rescue of G1 cyclin (Cln) function in yeast ...
Other than Rb, viral cyclin D-Cdk6 complex also targets p27Kip, a Cdk inhibitor of cyclin E and A. In addition, viral cyclin D- ... The phosphorylation of Rb by cyclin A-Cdk2, cyclin B-Cdk1, and cyclin E-Cdk2 are unaffected. The C terminus has a stretch of 21 ... In mice and humans, two more cyclin D proteins have been identified. The three homologues, called cyclin D1, cyclin D2, and ... among which is cyclin D. In this way, cyclin D is synthesized as long as the growth factor is present. Cyclin D levels in ...
Cyclins function as regulators of cyclin-dependent kinases. Different cyclins exhibit distinct expression and degradation ... Brooks AR, Shiffman D, Chan CS, Brooks EE, Milner PG (Apr 1996). "Functional analysis of the human cyclin D2 and cyclin D3 ... "The consensus motif for phosphorylation by cyclin D1-Cdk4 is different from that for phosphorylation by cyclin A/E-Cdk2". The ... G1/S-specific cyclin-D2 is a protein that in humans is encoded by the CCND2 gene. The protein encoded by this gene belongs to ...
Cyclins function as regulators of CDKs (cyclin-dependent kinase). Different cyclins exhibit distinct expression and degradation ... cyclin D1 is translocated to the IgH promoter leading to cyclin D1 overexpression. Chromosomal translocation of the cyclin D1 ... Cyclin D1 is a protein that in humans is encoded by the CCND1 gene. The CCND1 gene encodes the cyclin D1 protein. The human ... Cyclin D1 and the mechanisms it regulates have the potential to be a therapeutic target for cancer drugs: Cyclin D1 has been ...
"Cyclin K inhibits HIV-1 gene expression and replication by interfering with cyclin-dependent kinase 9 (CDK9)-cyclin T1 ... "Entrez Gene: CCNK cyclin K". Baek K, Brown RS, Birrane G, Ladias JA (February 2007). "Crystal structure of human cyclin K, a ... Cyclin K also interacts with HIV nef protein. In the presence of overexpressed Nef protein, Cyclin k and CDK9 binding is ... Cyclin K is indispensable for Leukemia growth. SETD1A, is also known to bind Cyclin K through its FLOS domain. The interaction ...
"Cyclin F regulates the nuclear localization of cyclin B1 through a cyclin-cyclin interaction". EMBO J. 19 (6): 1378-88. doi: ... G2/mitotic-specific cyclin-B1 is a protein that in humans is encoded by the CCNB1 gene. Cyclin B1 is a regulatory protein ... Like all cyclins, levels of cyclin B1 oscillate over the course of the cell cycle. Just prior to mitosis, a large amount of ... Cyclin B1 can reside in the nucleus or the cytoplasm which can have an effect on the malignant potential of cyclin B1 when ...
... is a protein that in humans is encoded by the CCNE2 gene. It is a G1 cyclin that binds Cdk2 and is inhibited by p27( ... Gudas JM, Payton M, Thukral S, Chen E, Bass M, Robinson MO, Coats S (January 1999). "Cyclin E2, a novel G1 cyclin that binds ... Zariwala, M.; Liu, J.; Xiong, Y. (1998-11-26). "Cyclin E2, a novel human G1 cyclin and activating partner of CDK2 and CDK3, is ...
Like all cyclin family members, cyclin E forms complexes with cyclin-dependent kinases. In particular, Cyclin E binds with CDK2 ... Cyclin E is a member of the cyclin family. Cyclin E binds to G1 phase Cdk2, which is required for the transition from G1 to S ... Cyclin E/CDK2 plays a critical role in the G1 phase and in the G1-S phase transition. Cyclin E/CDK2 phosphorylates ... Dysregulation of cyclin E occurs in 18-22% of the breast cancers. Cyclin E is a prognostic marker in breast cancer, its altered ...
Cyclins function as regulators of CDK kinases. Different cyclins exhibit distinct expression and degradation patterns that ... Cyclin-T1 is a protein that in humans is encoded by the CCNT1 gene. The protein encoded by this gene belongs to the highly ... This cyclin tightly associates with CDK9 kinase, and was found to be a major subunit of the transcription elongation factor p- ... This cyclin and its kinase partner were also found to be involved in the phosphorylation and regulation of the carboxy-terminal ...
Cyclin-A2 is a protein that in humans is encoded by the CCNA2 gene. It is one of the two types of cyclin A: cyclin A1 is ... Cyclin A2 belongs to the cyclin family, whose members regulate cell cycle progression by interacting with CDK kinases. Cyclin ... The cyclin A2-CDK2 complex eventually phosphorylates E2F, turning off cyclin A2 transcription. E2F promotes cyclin A2 ... Cyclin A2 is synthesized at the onset of S phase and localizes to the nucleus, where the cyclin A2-CDK2 complex is implicated ...
... has been shown to interact with P53, Cyclin-dependent kinase 7 and MNAT1. GRCh38: Ensembl release 89: ENSG00000134480 ... Cyclins function as regulators of CDK kinases. Different cyclins exhibit distinct expression and degradation patterns which ... Cyclin-H is a protein that in humans is encoded by the CCNH gene. The protein encoded by this gene belongs to the highly ... This cyclin forms a complex with CDK7 kinase and ring finger protein MAT1. The kinase complex is able to phosphorylate CDK2 and ...
... remains associated with CDK1 from late S into late G2 phase when it is replaced by cyclin B. Cyclin A/CDK1 is thought ... Cyclin A is the only cyclin that regulates multiple steps of the cell cycle. Cyclin A can regulate multiple cell cycle steps ... Cyclin A2 is expressed in dividing somatic cells. Cyclin A, along with the other members of the cyclin family, regulates cell ... P21 is a CDK inhibitor that binds to several cyclin/CDK complexes, including cyclin A-CDK2/1 and cyclin D/CDK4, and blocks the ...
Cyclin-dependent kinase 4, Cyclin-dependent kinase 6, EIF3K, and Retinoic acid receptor alpha. Cyclin Cyclin D GRCh38: Ensembl ... Cyclins function as regulators of CDK kinases. Different cyclins exhibit distinct expression and degradation patterns which ... Brooks AR, Shiffman D, Chan CS, Brooks EE, Milner PG (1996). "Functional analysis of the human cyclin D2 and cyclin D3 ... G1/S-specific cyclin-D3 is a protein that in humans is encoded by the CCND3 gene. The protein encoded by this gene belongs to ...
CDK6; cyclin D1, cyclin D2, cyclin D3 CDK7; cyclin H CDK8; cyclin C CDK9; cyclin T1, cyclin T2a, cyclin T2b, cyclin K CDK10 ... cyclin A, cyclin B CDK2; cyclin A, cyclin E CDK3; cyclin C CDK4; cyclin D1, cyclin D2, cyclin D3 CDK5; CDK5R1, CDK5R2. See also ... Furthermore, cyclin binding determines the specificity of the cyclin-CDK complex for particular substrates. Cyclins can ... Viruses can encode proteins with sequence homology to cyclins. One much-studied example is K-cyclin (or v-cyclin) from Kaposi ...
E2F.2FpRb complexes Hyperphosphorylation cdc25 Maturation promoting factor CDK cyclin A cyclin B cyclin D cyclin E Wee (cell ... "Cyclin F regulates the nuclear localization of cyclin B1 through a cyclin-cyclin interaction". EMBO J. 19 (6): 1378-1388. doi: ... Cyclin binding alters access to the active site of Cdk1, allowing for Cdk1 activity; furthermore, cyclins impart specificity to ... Furthermore, cyclins can target Cdk1 to particular subcellular locations. In addition to regulation by cyclins, Cdk1 is ...
"Entrez Gene: CDK10 cyclin-dependent kinase (CDC2-like) 10". Kasten M, Giordano A (Apr 2001). "Cdk10, a Cdc2-related kinase, ... Cyclin-dependent kinase 10 has been shown to interact with ETS2. GRCh38: Ensembl release 89: ENSG00000185324 - Ensembl, May ...
A Cyclin-dependent kinase 6 interacts with: CDKN2C, Cyclin D1, Cyclin D3, P16, PPM1B, and PPP2CA. Cell cycle Cyclin-dependent ... It is regulated by cyclins, more specifically by Cyclin D proteins and Cyclin-dependent kinase inhibitor proteins. The protein ... 2003). "Expression of Cyclin-Dependent Kinase 6, but Not Cyclin-Dependent Kinase 4, Alters Morphology of Cultured Mouse ... Kozar K, Sicinski P (March 2005). "Cell cycle progression without cyclin D-CDK4 and cyclin D-CDK6 complexes". Cell Cycle. ...
... has been shown to interact with: BRCA1, CDK2AP1, CDKN1B CDKN3, CEBPA, Cyclin A1, Cyclin E1, Flap ... "Entrez Gene: CDK2 cyclin-dependent kinase 2". Echalier A, Endicott JA, Noble ME (March 2010). "Recent developments in cyclin- ... This protein associates with and is regulated by the regulatory subunits of the complex including cyclin E or A. Cyclin E binds ... Lacy S, Whyte P (May 1997). "Identification of a p130 domain mediating interactions with cyclin A/cdk 2 and cyclin E/cdk 2 ...
... has been shown to interact with: Androgen receptor, Cyclin H, GTF2H1, MNAT1, P53, SUPT5H, and XPB. ... Cyclin-dependent kinase 7, or cell division protein kinase 7, is an enzyme that in humans is encoded by the CDK7 gene. The ... The growth suppressor p53 has been shown to interact with cyclin H both in vitro and in vivo. Addition of wild type p53 was ... "Entrez Gene: CDK7 cyclin-dependent kinase 7 (MO15 homolog, Xenopus laevis, cdk-activating kinase)". Patel H, Abduljabbar R, Lai ...
"OMIM Entry - * 123831 - CYCLIN-DEPENDENT KINASE 5; CDK5". omim.org. Retrieved 2020-11-02. Tsai, Li-Huei. Cyclin Dependent ... Cyclin-dependent kinase 5 is a protein, and more specifically an enzyme, that is encoded by the Cdk5 gene. It was discovered 15 ... Cyclin-Dependent+Kinase+5 at the U.S. National Library of Medicine Medical Subject Headings (MeSH) CDK5 human gene location in ... Cyclin Dependent Kinase 5. Springer. 19 August 2008. ISBN 978-0-387-78886-9. Patrick GN, Zukerberg L, Nikolic M, de la Monte S ...
During G2 phase, cyclin A is degraded, while cyclin B is synthesized and cyclin B-Cdk1 complexes form. Not only are cyclin B- ... cyclin-dependent kinase (CDK), with a regulatory subunit, cyclin. Once cyclin-dependent kinases bind to cyclin, the formed ... Cyclin Cyclin-dependent kinase Malumbres M, Barbacid M. Mammalian cyclin-dependent kinases. Trends Biochem. Sci. 2005 Nov;30(11 ... cyclin D1-Cdk4 and cyclin D1-Cdk6 phosphorylate pRB, followed by additional phosphorylation from the cyclin E-Cdk2 CDKC. Once ...
"Entrez Gene: CDK4 cyclin-dependent kinase 4". "CDK4 - Cyclin-dependent kinase 4 - Homo sapiens (Human) - CDK4 gene & protein". ... 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 ... 1995). "Identification of human cyclin-dependent kinase 8, a putative protein kinase partner for cyclin C". Proc. Natl. Acad. ...
... or CDK9 is a cyclin-dependent kinase associated with P-TEFb. The protein encoded by this gene is a ... This protein forms a complex with and is regulated by its regulatory subunit cyclin T or cyclin K. HIV-1 Tat protein was found ... Cyclin-Dependent+Kinase+9 at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Drosophila Cyclin dependent ... "Entrez Gene: CDK9 cyclin-dependent kinase 9 (CDC2-related kinase)". MacLachlan TK, Sang N, De Luca A, Puri PL, Levrero M, ...
"Entrez Gene: CDK3 cyclin-dependent kinase 3". Bullrich F, MacLachlan TK, Sang N, et al. (1995). "Chromosomal mapping of members ... 2002). "ik3-1/Cables is a substrate for cyclin-dependent kinase 3 (cdk 3)". Eur. J. Biochem. 268 (23): 6076-82. doi:10.1046/j. ... Ren S, Rollins BJ (2004). "Cyclin C/cdk3 promotes Rb-dependent G0 exit". Cell. 117 (2): 239-51. doi:10.1016/S0092-8674(04)00300 ... CDK3 can phosphorylate histone H1 and interacts with an unknown type of cyclin. GRCh38: Ensembl release 89: ENSG00000250506 - ...
Cyclin D / CDK4, Cyclin D / CDK6, and Cyclin E / CDK2 - regulates transition from G1 to S phase. G2/M cyclins - essential for ... The rise in presence of G1/S cyclins is paralleled by a rise in S cyclins. G1 cyclins do not behave like the other cyclins, in ... G1 cyclins, G1/S cyclins, S cyclins, and M cyclins. This division is useful when talking about most cell cycles, but it is not ... Note that the cyclins are now classified according to their conserved cyclin box structure, and not all these cyclins alter in ...
The model is based on a bicyclic phosphorylation-dephosphorylation cascade involving cyclin and cdc2 kinase. By constructing ... The model is based on a bicyclic phosphorylation-dephosphorylation cascade involving cyclin and cdc2 kinase. By constructing ...
Conserved Protein Domain Family CYCLIN_CCNH_rpt1, CCNH, also called MO15-associated protein, p34, or p37, is normally ... associated with the cyclin-dependent kinase cdk7, the catalytic subunit of the CDK-activating kinase (CAK) enzymatic complex ... first cyclin box found in cyclin-H (CCNH) and similar proteins. CCNH, also called MO15-associated protein, p34, or p37, is ... CCNH contains two cyclin boxes. This model corresponds to the first one. The cyclin box is a protein binding domain. ...
Free download of Cyclin Font. Released in 2000 by Apostrophic Lab and licensed for personal and commercial-use. Click now to ...
... regulates expression of cyclin D1. Furthermore, the group showed that many cancer patients encode a form of cyclin D1 that ... Protien Cyclin D1 governs microRNA processing in breast cancer. Date:. November 29, 2013. Source:. Thomas Jefferson University ... Cyclin D1, a protein that helps push a replicating cell through the cell cycle also mediates the processing and generation of ... Because the cyclin D1 gene has been implicated in a variety of other human cancers these findings may have broad implications ...
The Cyclin D-Cdk4,6/INK4/Rb/E2F pathway plays a key role in controlling cell growth by integrating multiple mitogenic and ... Cyclin D-dependent kinases, INK4 inhibitors and cancer Biochim Biophys Acta. 2002 Mar 14;1602(1):73-87. doi: 10.1016/s0304-419x ... The Cyclin D-Cdk4,6/INK4/Rb/E2F pathway plays a key role in controlling cell growth by integrating multiple mitogenic and ... vast majority of human tumors by genetic and epigenetic alterations that target at least some of its key members such as Cyclin ...
Neither DmCdc2, DmCdc2c (alias DmCdk2), cyclin A, nor cyclin B co-sedimented with cyclin C. They were present in complexes in ... Because analysis of the same embryos with cyclin A and cyclin B antisera revealed mitotic destruction of these cyclins, it ... Drosophila Cdk8, a kinase partner of cyclin C that interacts with the large subunit of RNA polymerase II. A number of cyclins ... Cyclin C: Biological Overview , References Gene name - Cyclin C Synonyms - Cytological map position - 88D6-88D6 Function - ...
Learn about Cyclin A at online-medical-dictionary.org ... Cyclin, Type A. Cyclins, Type A. E1A p60. Type A Cyclin. Type A ... A cyclin subtype that has specificity for CDC2 PROTEIN KINASE and CYCLIN-DEPENDENT KINASE 2. It plays a role in progression of ... Cyclin A. Synonyms. Adenovirus E1A Associated Protein p60. Adenovirus E1A-Associated Protein p60. ...
View mouse Cdk15 Chr1:59296029-59391656 with: phenotypes, sequences, polymorphisms, proteins, references, function
David Bartels lab contains the insert Cyclin D2 and is published in Cell. 2009 Aug 21. 138(4):673-84. This plasmid is ... Plasmid pMSCV Cyclin D2 long-wt from Dr. ... pMSCV Cyclin D2 long-wt was a gift from David Bartel (Addgene ...
View mouse Cdk9 Chr2:32595796-32603088 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
Cyclin D1 from Neuroscience News features breaking science news from research labs, scientists and colleges around the world. ...
Protein target information for Cyclin 1 (Plasmodium falciparum 3D7). Find diseases associated with this biological target and ...
View Mouse Monoclonal anti-Cyclin H Antibody (1B8) (H00000902-M01). Validated Applications: WB, ELISA, ICC/IF, IHC. Validated ... Reviews for Cyclin H Antibody (H00000902-M01) (0) There are no reviews for Cyclin H Antibody (H00000902-M01). By submitting a ... Blogs on Cyclin H. There are no specific blogs for Cyclin H, but you can read our latest blog posts. ... Diseases for Cyclin H Antibody (H00000902-M01). Discover more about diseases related to Cyclin H Antibody (H00000902-M01). ...
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STRUCTURE OF HUMAN THR160-PHOSPHO CDK2-CYCLIN A COMPLEXED WITH A BISANILINOPYRIMIDINE INHIBITOR ... Dissecting the Determinants of Cyclin-Dependent Kinase 2 and Cyclin-Dependent Kinase 4 Inhibitor Selectivity.. Pratt, D.J., ... Cyclin dependent kinases are a key family of kinases involved in cell cycle regulation and are an attractive target for cancer ... Cyclin dependent kinases are a key family of kinases involved in cell cycle regulation and are an attractive target for cancer ...
Structure of human Thr160-phospho CDK2/cyclin A complexed with the inhibitor NU6086 ... Structure-based design of a potent purine-based cyclin-dependent kinase inhibitor.. Davies, T.G., Bentley, J., Arris, C.E., ... Aberrant control of cyclin-dependent kinases (CDKs) is a central feature of the molecular pathology of cancer. Iterative ... Aberrant control of cyclin-dependent kinases (CDKs) is a central feature of the molecular pathology of cancer. Iterative ...
Cyclin I is an atypical cyclin because it is most abundant in postmitotic cells. We previously showed that cyclin I does not ... we investigated the mechanism by which cyclin I safeguards against apoptosis and found that cyclin I bound and activated cyclin ... or p35/cyclin I (lanes 4, 8). (. B. ) To compare the kinase kinetics by which cyclin I-Cdk5 phosphorylates tau in comparison ... Cyclin I-Cdk5 showed phosphorylation kinetics similar to those of p35-Cdk5. Phosphorylation of tau was already evident after 5 ...
The expression of Cyclin D1 mRNA was detected by qRT-PCR. The expression of Cyclin D1 protein was detected by enzyme-linked ... Downregulation of miR-4755-5p promotes fluoride-induced osteoblast activation via tageting Cyclin D1.. Author: Gao J, Qin Y, ... Based on our previous miRNA sequence results, bioinformatic analysis was used to predict miR-4755-5p targeting Cyclin D1. ... The relative miR-4755-5p expression showed a negative correlation with Cyclin D1 expression. Subsequently, in human osteoblasts ...
With kids bikes from balance bikes, first pedal bikes, hybrid bikes to mountain & road bikes, Rutland Cycling has a huge choice of Frog bikes available.
Rabbit Monoclonal Cyclin D1 antibody [RM241]. Validated in WB, IHC-P. Tested in Human. ... Cyclins function as regulators of CDK kinases. Different cyclins exhibit distinct expression and degradation patterns which ... This cyclin forms a complex with and functions as a regulatory subunit of CDK4 or CDK6, whose activity is required for cell ... There are currently no references for Cyclin D1 antibody [RM241] (GTX33611). Be the first to share your publications with this ...
The cyclin-dependent kinase inhibitor AT7519 accelerates neutrophil apoptosis in sepsis-related acute respiratory distress ... The cyclin-dependent kinase inhibitor AT7519 accelerates neutrophil apoptosis in sepsis-related acute respiratory distress ... While the cyclin-dependent kinase inhibitor AT7519 induces neutrophil apoptosis to promote inflammation resolution in ... highlighting cyclin-dependent kinase inhibitors as potential novel therapeutic agents. ...
ELM data can be downloaded & distributed for non-commercial use according to the ELM Software License Agreement ...
Regulation of cyclin-substrate docking by a G1 arrest signaling pathway and the Cdk inhibitor Far1. Curr Biol. 2014 Jun 16; 24( ... "Cyclins" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject Headings) ... Ishidate T, Elewa A, Kim S, Mello CC, Shirayama M. Divide and differentiate: CDK/Cyclins and the art of development. Cell Cycle ... Notch signaling mediates G1/S cell-cycle progression in T cells via cyclin D3 and its dependent kinases. Blood. 2009 Feb 19; ...
In this study, we evaluated cyclin D1, D2 and D3 protein expression in AL amyloidosis, and compared cyclin D positivity to ... Cyclin D dysregulation has been proposed to be a common mechanism in PC disorders, as in multiple myeloma; the majority of ... patients have dysregulated cyclin D expression.6 This has not been extensively investigated in AL amyloidosis. ...
Expression profile analysis revealed sik1 as part of a genetic network that controls the cell cycle, where the cyclin-dependent ...
... cyclin D3, inhibition of CDK6 or cyclin D3 induces apoptosis. The mechanisms underlying the prosurvival function of cyclin D3- ... were directly phosphorylated and inhibited by cyclin D3-CDK6, suggesting that cyclin D3-CDK6 may have a unique role in glucose ... Inhibitors of the cyclin-dependent kinases CDK4 and CDK6 induce cell-cycle arrest in RB1-proficient tumors and have had ... Major finding: Cyclin D3-CDK6 inhibits the glycolytic enzymes PFK1 and PKM2 to prevent T-ALL cell apoptosis. ...
Here, we dissected the pathways that are responsible for EMT in cells deficient for Cyclin A2. In Cyclin A2-depleted normal ... Cyclin A2 modulates EMT via beta-catenin and phospholipase C pathways. Cheung, C. T.; Bendris, N.; Paul, C.; Hamieh, A.; Anouar ... We have previously demonstrated that Cyclin A2 is involved in cytoskeletal dynamics, epithelial-mesenchymal transition (EMT) ... Our findings will broaden our knowledge on how Cyclin A2 contributes to EMT and metastasis. ...
Cyclin-dependent kinase 5, Munc18a and Munc18-interacting protein 1/X11α protein up-regulation in Alzheimers disease. ... Cyclin-dependent kinase 5 and its activator p35 disrupt Munc18a-syntaxin 1 binding, thereby promoting synaptic vesicle fusion ... Jacobs, E.H, Williams, R.J, & Francis, P.T. (2006). Cyclin-dependent kinase 5, Munc18a and Munc18-interacting protein 1/X11α ... We investigated protein levels of the signaling pathway: p35, cyclin-dependent kinase 5, Munc18a, syntaxin 1A and 1B, Munc18- ...
We then studied the effect of Dox on the p34cdc2/cyclin B1 complex because it plays a key role in regulating G2/M phase ... In contrast, Dox treatment was found to induced cyclin B1 accumulation as a result of stimulating its synthesis and inhibiting ... Cell cycle-dependent cytotoxicity, G2/M phase arrest, and disruption of p34cdc2/cyclin B1 activity induced by doxorubicin in ... Cell cycle-dependent cytotoxicity, G2/M phase arrest, and disruption of p34cdc2/cyclin B1 activity induced by doxorubicin in ...
  • Cyclins, when bound with the dependent kinases, such as the p34/cdc2/cdk1 protein, form the maturation-promoting factor. (wikipedia.org)
  • Cyclins function as regulators of CDK kinases. (novusbio.com)
  • Cyclin dependent kinases are a key family of kinases involved in cell cycle regulation and are an attractive target for cancer chemotherapy. (rcsb.org)
  • Aberrant control of cyclin-dependent kinases (CDKs) is a central feature of the molecular pathology of cancer. (rcsb.org)
  • A large family of regulatory proteins that function as accessory subunits to a variety of CYCLIN-DEPENDENT KINASES. (umassmed.edu)
  • Notch signaling mediates G1/S cell-cycle progression in T cells via cyclin D3 and its dependent kinases. (umassmed.edu)
  • Inhibitors of the cyclin-dependent kinases CDK4 and CDK6 induce cell-cycle arrest in RB1-proficient tumors and have had promising results in several tumor types. (aacrjournals.org)
  • Cyclin-dependent kinases (Cdks) are principal drivers of cell division and are an important therapeutic target to inhibit aberrant proliferation. (escholarship.org)
  • Cyclin D1 antibody is a regulatory subunit of certain protein kinases thought to advance the G1 phase of the cell cycle. (micro-shop.pl)
  • The eukaryotic cell cycle comprises a series of events, whose ordering and correct progression depends on the oscillating activity of cyclin-dependent kinases (Cdks), which safeguard timely duplication and segregation of the genome. (unimi.it)
  • Regulation of the DNA damage response by cyclin-dependent kinases / C. Trovesi, N. Manfrini, M. Falcettoni, M.P. Longhese. (unimi.it)
  • A relatively well understood example is the network that controls progression of the cell cycle, where cyclin-dependent kinases (CDKs) couple with various cyclins over the cell cycle to regulate critical processes [ 2 - 4 ]. (biomedcentral.com)
  • Protein kinases that control cell cycle progression in all eukaryotes and require physical association with CYCLINS to achieve full enzymatic activity. (bvsalud.org)
  • Cyclin-dependent kinases are regulated by phosphorylation and dephosphorylation events. (bvsalud.org)
  • Cyclins themselves have no enzymatic activity but have binding sites for some substrates and target the Cdks to specific subcellular locations. (wikipedia.org)
  • Cyclin is a family of proteins that controls the progression of a cell through the cell cycle by activating cyclin-dependent kinase (CDK) enzymes or group of enzymes required for synthesis of cell cycle. (wikipedia.org)
  • For example, the amino-terminal regions of S and M cyclins contain short destruction-box motifs that target these proteins for proteolysis in mitosis. (wikipedia.org)
  • The work supports the idea that cancer-causing proteins like cyclin D1 may drive cancer progression in part via miRNA biogenesis. (sciencedaily.com)
  • In addition, levels of the prosurvival proteins Bcl-2 and Bcl-XL were reduced in podocytes and neurons from cyclin I-deficient mice, and restoration of Bcl-2 or Bcl-XL expression prevented injury-induced apoptosis. (jci.org)
  • Taken together, these data suggest that a cyclin I-Cdk5 complex forms a critical antiapoptotic factor in terminally differentiated cells that functions via MAPK signaling to modulate levels of the prosurvival proteins Bcl-2 and Bcl-XL. (jci.org)
  • 1992, 1993) that the p34cdc2/cyclin B complex associates with microtubules in the mitotic spindle and premeiotic aster in starfish oocytes, and that microtubule-associated proteins (MAPs) might be responsible for this interaction. (rupress.org)
  • We show that cyclin-dependent kinase (CDK) consensus motifs are frequently clustered in CDK substrate proteins. (biomedcentral.com)
  • Cyclins are a family of proteins that control how cells proceed through the multi-step cycle of cell division. (medlineplus.gov)
  • A cyclin forms a complex with Cdk, which begins to activate but the complete activation requires phosphorylation, as well. (wikipedia.org)
  • The model is based on a bicyclic phosphorylation-dephosphorylation cascade involving cyclin and cdc2 kinase. (ebi.ac.uk)
  • Cyclin I-Cdk5 showed phosphorylation kinetics similar to those of p35-Cdk5. (jci.org)
  • Bhaduri S, Valk E, Winters MJ, Gruessner B, Loog M, Pryciak PM. A docking interface in the cyclin Cln2 promotes multi-site phosphorylation of substrates and timely cell-cycle entry. (umassmed.edu)
  • In mitosis, Cyclin B1 undergoes phosphorylation at several sites, a subset of which have been proposed to play a role in Cyclin B1 accumulation in the nucleus. (duke.edu)
  • thus, we propose that Cyclin B1 phosphorylation at the G2/M transition prevents its interaction with CRM1, thereby reducing nuclear export and facilitating nuclear accumulation. (duke.edu)
  • The oscillations of the cyclins, namely fluctuations in cyclin gene expression and destruction by the ubiquitin mediated proteasome pathway, induce oscillations in Cdk activity to drive the cell cycle. (wikipedia.org)
  • Dr. Pestell and colleagues developed transgenic mice that could induce cyclin D1 expression in the breast and examined cells with cyclin D1 gene deleted. (sciencedaily.com)
  • Because the cyclin D1 gene has been implicated in a variety of other human cancers these findings may have broad implications for processing of non coding RNA in human tumorigenesis. (sciencedaily.com)
  • The protein encoded by this gene belongs to the highly conserved cyclin family, whose members are characterized by a dramatic periodicity in protein abundance through the cell cycle. (novusbio.com)
  • 1983 Subsequently cyclin A genes have been found in all multicellular organisms including humans (Pines and Hunter 1990 While only a single cyclin A gene is present in the genomes of and cultured fibroblasts XI-006 or other cell types blocked DNA synthesis consistent with the essential function for cyclin A in DNA replication (Girard et al. (immune-source.com)
  • RESULTS Generation and Characterization of Conditional Cyclin A2 Knockout Mice To obtain a conditional cyclin A2 allele we inserted sites into the first and seventh intron of the murine cyclin A2 gene (Physique 1A). (immune-source.com)
  • The gene-targeting construct was launched into embryonal stem (ES) cells and heterozygous cyclin A2f/+ (Af denotes XI-006 the "floxed" allele) ES were obtained through homologous recombination (Figures 1A and 1B). (immune-source.com)
  • The CCND2 gene provides instructions for making a protein called cyclin D2. (medlineplus.gov)
  • The molecular consequence of translocation is overexpression of the protein cyclin D1 (coded by the PRAD1 gene located close to the breakpoint). (medscape.com)
  • S cyclins bind to Cdk and the complex directly induces DNA replication. (wikipedia.org)
  • In addition to its role in regulating the cell cycle, cyclin D1 induces Dicer and thereby promotes the maturation of miRNA," says lead researcher Richard Pestell, M.D., Ph.D., Director of the Kimmel Cancer Center at Thomas Jefferson University and Chair of the Department of Cancer Biology. (sciencedaily.com)
  • While the cyclin-dependent kinase inhibitor AT7519 induces neutrophil apoptosis to promote inflammation resolution in preclinical models of lung inflammation, its potential efficacy in ARDS has not been examined. (bmj.com)
  • However, in T-cell acute lymphoblastic leukemia (T-ALL), which predominately expresses CDK6 and the activating cyclin, cyclin D3, inhibition of CDK6 or cyclin D3 induces apoptosis. (aacrjournals.org)
  • Functionally, miR-193b induces a G1 cell cycle arrest and cell death in neuroblastoma cell lines by reducing the expression of MYCN , Cyclin D1 and MCL-1 , three important oncogenes in neuroblastoma of which inhibition has shown promising results in preclinical testing. (oncotarget.com)
  • In the current study, the group sought to investigate the mechanism by which cyclin D1 regulates the biogenesis of non coding miRNA. (sciencedaily.com)
  • Here, we investigated the mechanism by which cyclin I safeguards against apoptosis and found that cyclin I bound and activated cyclin-dependent kinase 5 (Cdk5) in isolated mouse podocytes and neurons. (jci.org)
  • F-box protein specificity for g1 cyclins is dictated by subcellular localization. (umassmed.edu)
  • Spy1 lacks the cyclin-binding site that mediates p27 and substrate affinity, explaining why Cdk-Spy1 is poorly inhibited by p27 and lacks specificity for substrates with cyclin-docking sites. (escholarship.org)
  • We previously showed that cyclin I does not regulate proliferation, but rather controls survival of podocytes, terminally differentiated epithelial cells that are essential for the structural and functional integrity of kidney glomeruli. (jci.org)
  • Further, the results of miR-4755-5p mimic transfection confirmed that under the action of NaF, miR-4755-5p overexpression reduced Cyclin D1 protein expression within osteoblasts and further inhibited cell proliferation and activation. (fluoridealert.org)
  • cyclin A function was essential for proliferation of hematopoietic and embryonal stem cells. (immune-source.com)
  • 1997 In the work explained below we decided to revisit the requirement for cyclin A function in cell proliferation using conditional cyclin A knockout mice. (immune-source.com)
  • EP12] shows some positive staining reaction in B-cell chromic lymphocytic leukemia proliferation not seen with other Cyclin D1 clones. (micro-shop.pl)
  • Cyclin D2's role in the cell division cycle makes it a key controller of the rate of cell growth and division (proliferation) in the body. (medlineplus.gov)
  • The resulting buildup of cyclin D2 in cells triggers them to continue dividing when they otherwise would not have, leading to abnormal cell proliferation. (medlineplus.gov)
  • It is less clear how a buildup of cyclin D2 contributes to polydactyly, although the extra digits are probably related to abnormal cell proliferation in the developing hands and feet. (medlineplus.gov)
  • We found that BSW shMSLN cells had decreased cyclin E, and their proliferation rate was reverted to nearly that of untransformed cells. (cdc.gov)
  • Immunocytochemistry/ Immunofluorescence: Cyclin H Antibody (1B8) [H00000902-M01] - Analysis of monoclonal antibody to CCNH on HeLa cell. (novusbio.com)
  • Immunohistochemistry-Paraffin: Cyclin H Antibody (1B8) [H00000902-M01] - Analysis of monoclonal antibody to CCNH on formalin-fixed paraffin-embedded human testis. (novusbio.com)
  • Western Blot: Cyclin H Antibody (1B8) [H00000902-M01] - CCNH monoclonal antibody (M01), clone 1B8 Analysis of CCNH expression in HeLa. (novusbio.com)
  • Sandwich ELISA: Cyclin H Antibody (1B8) [H00000902-M01] - Detection limit for recombinant GST tagged CCNH is approximately 1ng/ml as a capture antibody. (novusbio.com)
  • WB analysis of HeLa cell lysate using GTX33611 Cyclin D1 antibody [RM241]. (genetex.com)
  • IHC-P analysis of human tonsil tissue using GTX33611 Cyclin D1 antibody [RM241]. (genetex.com)
  • There are currently no references for Cyclin D1 antibody [RM241] (GTX33611) . (genetex.com)
  • This rabbit monoclonal antibody recognizes a protein of 36 kDa, identified as Cyclin D1 antibody (also known as Bcl-1 or PRAD-1). (micro-shop.pl)
  • Cyclin D1 Antibody / Ccnd1, supplied by NSJ Bioreagents, used in various techniques. (bioz.com)
  • CCNH, also called MO15-associated protein, p34, or p37, is normally associated with the cyclin-dependent kinase cdk7, the catalytic subunit of the CDK-activating kinase (CAK) enzymatic complex. (nih.gov)
  • Dysregulation of CDK8 (Cyclin-Dependent Kinase 8) and its regulatory partner CycC (Cyclin C) , two subunits of the conserved Mediator (MED) complex, have been linked to diverse human diseases such as cancer. (sdbonline.org)
  • Assay of the mutants with a cyclin-dependent kinase 4-selective bisanilinopyrimidine shows that the K89T mutation is primarily responsible for the selectivity of this compound. (rcsb.org)
  • Use of the cyclin-dependent kinase 2-selective 6-cyclohexylmethoxy-2-(4'-sulfamoylanilino)purine (NU6102) shows that K89T has no role in the selectivity, while the remaining three mutations have a cumulative influence. (rcsb.org)
  • cyclin-dependent kinase 5, regulatory. (wikigenes.org)
  • We demonstrate the first pharmacological compound to induce neutrophil apoptosis in sepsis-related ARDS, highlighting cyclin-dependent kinase inhibitors as potential novel therapeutic agents. (bmj.com)
  • Cyclin-dependent kinase 5 and its activator p35 disrupt Munc18a-syntaxin 1 binding, thereby promoting synaptic vesicle fusion during exocytosis. (eur.nl)
  • We investigated protein levels of the signaling pathway: p35, cyclin-dependent kinase 5, Munc18a, syntaxin 1A and 1B, Munc18-interacting protein 1 and Munc18-interacting protein 2 in Alzheimer's disease cortex and found that this pathway was up-regulated in the Alzheimer's disease parietal and occipital cortex. (eur.nl)
  • Cell cycle-dependent cytotoxicity, G2/M phase arrest, and disruption of p34cdc2/cyclin B1 activity induced by doxorubicin in synchronized P388 cells. (aspetjournals.org)
  • Our results suggest that anthracycline-induced cytotoxicity is cell cycle dependent and is mediated, at least in part, by disturbance of the regulation of p34cdc2/cyclin B1 complex, thus leading to G2/M phase arrest. (aspetjournals.org)
  • In these compartments cyclin A-Cdk complexes are expressed at particularly high levels which may render stem cells dependent on cyclin A. INTRODUCTION Replication of genetic material during cell division in Metazoan organisms is thought to be driven by cyclin A. Cyclin A was the first cyclin cloned in any organism (Swenson et al. (immune-source.com)
  • DHA-enriched fish oil upregulates cyclin-dependent kinase inhibitor 2A (P16 INK ) expression and downregulates telomerase activity without modulating effects of PPARγ Pro12Ala polymorphism in type 2 diabetic patients: A randomized, double-blind, placebo-controlled clinical trial. (bvsalud.org)
  • The more aggressive basal-like subtype of breast cancers, however, exhibited lower levels of cyclin D1 and Dicer, which would in turn globally reduce the level of mature miRNA. (sciencedaily.com)
  • High levels of cyclin D3 and CDK6 may predict response to CDK4/6 inhibitors in multiple tumor types. (aacrjournals.org)
  • Together, these findings elucidate a prosurvival role for cyclin D3-CDK6 in metabolism, in addition to its role in cell-cycle progression, and suggest that high levels of cyclin D3 and CDK6 may predict response to CDK4/6 inhibitors. (aacrjournals.org)
  • 1986 and injection of anti-cyclin A2 antibodies into cultured fibroblasts or inhibiting cyclin A2 function by p21Cip1 during the G2 phase blocked G2?M phase progression (Furuno et al. (immune-source.com)
  • Double staining of primate cells with anti-cyclin B and anti-MAP4 antibodies demonstrated these two antigens were colocalized on microtubules and copartitioned following two treatments that altered MAP4 distribution. (rupress.org)
  • The mechanism by which MSLN contributes to these more aggressive behaviors was investigated by using ingenuity pathway analysis, which predicted that increased MSLN could induce cyclin E expression. (cdc.gov)
  • Cdk enzymatic activity is tightly controlled through cyclin interactions, posttranslational modifications, and binding of inhibitors such as the p27 tumor suppressor protein. (escholarship.org)
  • The Cyclin D-Cdk4,6/INK4/Rb/E2F pathway plays a key role in controlling cell growth by integrating multiple mitogenic and antimitogenic stimuli. (nih.gov)
  • This pathway is deregulated in the vast majority of human tumors by genetic and epigenetic alterations that target at least some of its key members such as Cyclin D1, Cdk4, INK4a and INK4b, pRb etc. (nih.gov)
  • Pope PA, Bhaduri S, Pryciak PM. Regulation of cyclin-substrate docking by a G1 arrest signaling pathway and the Cdk inhibitor Far1. (umassmed.edu)
  • Components of the canonical wingless (WNT) pathway, including WNT8b, WNT10a, WNT10b, frizzled 1 and 2 and TCF4 were upregulated at the messenger RNA and protein levels following Cyclin A2 depletion. (cnrs.fr)
  • The cyclin D2 protein is regulated by a chemical signaling pathway called the PI3K-AKT-mTOR pathway. (medlineplus.gov)
  • However analyses of cell cycle progression using propidium iodide and anti-BrdU staining revealed that ablation of cyclin A2 increased the portion of cells in S and G2/M phases with concomitant decrease in the G1 populace (Figures 2C and 2D). (immune-source.com)
  • Scholars@Duke publication: Control of cyclin B1 localization through regulated binding of the nuclear export factor CRM1. (duke.edu)
  • Cyclin B1 localization changes dramatically during the cell cycle, precipitously transiting from the cytoplasm to the nucleus at the beginning of mitosis. (duke.edu)
  • We show here that the previously characterized cytoplasmic retention sequence of Cyclin B1, responsible for its interphase cytoplasmic localization, is actually an autonomous nuclear export sequence, capable of directing nuclear export of a heterologous protein, and able to bind specifically to the recently identified export mediator, CRM1. (duke.edu)
  • We propose that the observed cytoplasmic localization of Cyclin B1 during interphase reflects the equilibrium between ongoing nuclear import and rapid CRM1-mediated export. (duke.edu)
  • Activation of the Cyclin B/Cdc2 kinase complex triggers entry into mitosis in all eukaryotic cells. (duke.edu)
  • They found that patients with the luminal A subtype of breast cancer had increased levels of expression of both cyclin D1 and Dicer. (sciencedaily.com)
  • A widely-expressed cyclin A subtype that functions during the G1/S and G2/M transitions of the CELL CYCLE. (uams.edu)
  • Expression of cyclins detected immunocytochemically in individual cells in relation to cellular DNA content (cell cycle phase), or in relation to initiation and termination of DNA replication during S-phase, can be measured by flow cytometry. (wikipedia.org)
  • In prior work, they showed that cyclin D1 regulates the non coding genome, and that the non-coding genome, in turn, regulates expression of cyclin D1. (sciencedaily.com)
  • Different cyclins exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. (novusbio.com)
  • The expression of Cyclin D1 mRNA was detected by qRT-PCR. (fluoridealert.org)
  • The expression of Cyclin D1 protein was detected by enzyme-linked immunosorbent assay (ELISA) and Western blotting, respectively. (fluoridealert.org)
  • In the fluoride-exposed population, the results showed that with the increase in UF content, the expression of miR-4755-5p decreased gradually, while the mRNA transcription and protein expression of Cyclin D1 increased gradually. (fluoridealert.org)
  • The relative miR-4755-5p expression showed a negative correlation with Cyclin D1 expression. (fluoridealert.org)
  • Subsequently, in human osteoblasts treated with sodium fluoride (NaF), the results also showed that NaF caused low expression of miR-4755-5p and increased expression of Cyclin D1 . (fluoridealert.org)
  • The results demonstrate that fluoride exposure induced the downregulation of miR-4755-5p and downregulated miR-4755-5p promoted fluoride-induced osteoblast activation by increasing Cyclin D1 protein expression. (fluoridealert.org)
  • the majority of patients have dysregulated cyclin D expression. (bmj.com)
  • In this study, we evaluated cyclin D1, D2 and D3 protein expression in AL amyloidosis, and compared cyclin D positivity to other conventional laboratory parameters as a diagnostic tool and as a potential biomarker for minimal residual disease. (bmj.com)
  • Moreover, in breast cancer cells, which express CDK4 instead of CDK6, palbociclib induced cell-cycle arrest instead of apoptosis, further indicating that expression of cyclin D3 and CDK6 in T-ALL cells promotes apoptosis in response to palbociclib. (aacrjournals.org)
  • Additionally, 16 of 18 nonleukemic cancer cell lines exhibiting high expression of cyclin D3 and CDK6 underwent apoptosis in response to palbociclib, and, in melanoma patient-derived xenografts, high cyclin D3 and CDK6 expression was associated with tumor regression after CDK4/6 inhibition. (aacrjournals.org)
  • Fibroblasts were isolated from cyclin A1-/-A2f/f embryos cultured and transduced with Cre-expressing viruses thereby ablating all cyclin A expression (Figures 1D and S1A). (immune-source.com)
  • Transient expression of cyclin D1 is sufficient to promote hepatocyte replication and liver growth in vivo. (laboratorynotes.com)
  • There are several different cyclins that are active in different parts of the cell cycle and that cause the Cdk to phosphorylate different substrates. (wikipedia.org)
  • A ) HEK293 cells were transfected with HA-Cdk5, then cotransfected with either myc-p35 or myc-cyclin I. Following an IP to the myc epitope tag on either p35 or cyclin I, in vitro kinase assays were performed using either histone H1 (HH1) or tau as substrates. (jci.org)
  • The mechanisms underlying the prosurvival function of cyclin D3-CDK6 have not been elucidated, prompting Wang and colleagues to search for substrates that may promote cancer cell survival. (aacrjournals.org)
  • The levels of S cyclins remain high, not only throughout S phase, but through G2 and early mitosis as well to promote early events in mitosis. (wikipedia.org)
  • M cyclin concentrations rise as the cell begins to enter mitosis and the concentrations peak at metaphase. (wikipedia.org)
  • The destruction of M cyclins during metaphase and anaphase, after the Spindle Assembly Checkpoint is satisfied, causes the exit of mitosis and cytokinesis. (wikipedia.org)
  • 1992 In addition cyclin A2 was postulated to play a role in access of cells into mitosis (Swenson et al. (immune-source.com)
  • Cyclin D1, when used in tandem with CD5, CD10 and CD23 may aid in the diagnosis for mantle cell lymphoma. (micro-shop.pl)
  • Cdk5 activity was reduced in glomeruli and brain lysates from cyclin I-deficient mice, and inhibition of Cdk5 increased in vitro the susceptibility to apoptosis in response to cellular damage. (jci.org)
  • Cyclin D3-CDK6 inhibits the glycolytic enzymes PFK1 and PKM2 to prevent T-ALL cell apoptosis. (aacrjournals.org)
  • CCNH contains two cyclin boxes. (nih.gov)
  • Our findings will broaden our knowledge on how Cyclin A2 contributes to EMT and metastasis. (cnrs.fr)
  • 6-phosphofructokinase (PFK1) and pyruvate kinase M2 (PKM2), enzymes that catalyze irreversible, rate-limiting steps in glycolysis, were directly phosphorylated and inhibited by cyclin D3-CDK6, suggesting that cyclin D3-CDK6 may have a unique role in glucose metabolism. (aacrjournals.org)
  • This cyclin forms a complex with and functions as a regulatory subunit of CDK4 or CDK6, whose activity is required for cell cycle G1/S transition. (genetex.com)
  • In Cyclin A2-depleted normal murine mammary gland (NMuMG) cells expressing RasV12, we found that beta-catenin was liberated from the cell membrane and cell-cell junctions and underwent nuclear translocation and activation. (cnrs.fr)
  • The first of which is the conserved cyclin box, outside of which cyclins are divergent. (wikipedia.org)
  • Cyclins were originally discovered by R. Timothy Hunt in 1982 while studying the cell cycle of sea urchins. (wikipedia.org)
  • Cyclins were originally named because their concentration varies in a cyclical fashion during the cell cycle. (wikipedia.org)
  • Note that the cyclins are now classified according to their conserved cyclin box structure, and not all these cyclins alter in level through the cell cycle. (wikipedia.org)
  • Cyclins can be divided into four classes based on their behaviour in the cell cycle of vertebrate somatic cells and yeast cells: G1 cyclins, G1/S cyclins, S cyclins, and M cyclins. (wikipedia.org)
  • The cyclins also promote other activities to progress the cell cycle, such as centrosome duplication in vertebrates or spindle pole body in yeast. (wikipedia.org)
  • G1 cyclins do not behave like the other cyclins, in that the concentrations increase gradually (with no oscillation), throughout the cell cycle based on cell growth and the external growth-regulatory signals. (wikipedia.org)
  • The presence of G cyclins coordinate cell growth with the entry to a new cell cycle. (wikipedia.org)
  • Cell changes in the cell cycle like the assembly of mitotic spindles and alignment of sister-chromatids along the spindles are induced by M cyclin- Cdk complexes. (wikipedia.org)
  • Cyclin A the first cyclin ever cloned is regarded as an essential component of the cell cycle engine. (immune-source.com)
  • 1997 These studies have led to the current model that this "core" components of the cell cycle machinery (cyclins A and B) symbolize XI-006 absolutely essential elements of the cell cycle engine (Hochegger et al. (immune-source.com)
  • Analyses of Cyclin A-null Fibroblasts We next derived fibroblasts from conditional cyclin A2 knockout embryos and cultured them culture (Physique 2A) and normally re-entered the cell cycle from quiescence (Physique 2B). (immune-source.com)
  • Bandyopadhyay S, Bhaduri S, ?rd M, Davey NE, Loog M, Pryciak PM. Comprehensive Analysis of G1 Cyclin Docking Motif Sequences that Control CDK Regulatory Potency In?Vivo. (umassmed.edu)
  • Physique 1 Generation of Cyclin A2f/f Mice In order to verify that deletion of the "floxed" cyclin A2 sequences resulted in a functionally null allele we crossed cyclin A2f/f mice with a "deleter" Meox2-Cre strain (Tallquist and Soriano 2000 and generated cyclin A2? (immune-source.com)
  • Hence deletion of the "floxed" cyclin A2 sequences converts the conditional cyclin A2 allele into a functionally null allele. (immune-source.com)
  • Each of the known mutations changes a single protein building block (amino acid) in the cyclin D2 protein. (medlineplus.gov)
  • De novo CCND2 mutations leading to stabilization of cyclin D2 cause megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome. (medlineplus.gov)
  • Kaposi sarcoma herpesvirus (KSHV) encodes a D-type cyclin (ORF72) that binds CDK6 and is likely to contribute to KSHV-related cancers. (wikipedia.org)
  • The metabolic function of cyclin D3-CDK6 kinase in cancer cell survival. (aacrjournals.org)
  • This cyclin forms a complex with CDK7 kinase and ring finger protein MAT1. (novusbio.com)
  • Simultaneously, luciferase reporter assays verified that Cyclin D1 was the miR-4755-5p direct target. (fluoridealert.org)
  • Using antisense RNA, Dr. Pestell's group was the first to show that cyclin D1 drives mammary tumor growth in vivo. (sciencedaily.com)
  • However, all members of the cyclin family are similar in 100 amino acids that make up the cyclin box. (wikipedia.org)
  • This cyclin and its kinase partner are components of TFIIH, as well as RNA polymerase II protein complexes. (novusbio.com)
  • Furthermore, we found that levels of phosphorylated MEK1/2 and ERK1/2 were decreased in cyclin I-deficient podocytes and that inhibition of MEK1/2 restored Bcl2 and Bcl-XL protein levels. (jci.org)
  • Cyclin D1 represses gluconeogenesis via inhibition of the transcriptional coactivator PGC1α. (laboratorynotes.com)
  • Finally, we examine co-clustering of the CDK consensus motifs with the 'cy' or RXL motif [ 17 ], which is known to be important in determining which CDK-cyclin complex will phosphorylate a given substrate. (biomedcentral.com)
  • The researchers noticed that cells lacking cyclin D1 produced less of the miRNA-processing protein, Dicer, and therefore had reduced levels of mature miRNA. (sciencedaily.com)
  • The group also examined cells lacking Dicer, and noted many similarities between Dicer-lacking and cyclin D1-lacking cells, in addition to failure of miRNA processing, suggesting a deeper connection between these two processes. (sciencedaily.com)
  • Cyclin I is an atypical cyclin because it is most abundant in postmitotic cells. (jci.org)
  • B ) To compare the kinase kinetics by which cyclin I-Cdk5 phosphorylates tau in comparison with p35-Cdk5, a time-course experiment was performed in HEK293 cells cotransfected with myc-p35 and HA-Cdk5 or myc-cyclin I and HA-Cdk5. (jci.org)
  • Here, we dissected the pathways that are responsible for EMT in cells deficient for Cyclin A2. (cnrs.fr)
  • Cyclin A2f/+ ES cells were then injected into mouse blastocysts and homozygous cyclin A2f/f animals were generated using standard procedures (Geng et al. (immune-source.com)
  • We found that cells lacking all A-type cyclins proliferated normally in culture (Physique XI-006 2A) and joined the S phase from G0. (immune-source.com)
  • In support of this hypothesis, we found that treatment of cells with leptomycin B, which disrupted Cyclin B1-CRM1 interactions, led to a marked nuclear accumulation of Cyclin B1. (duke.edu)
  • Tsunekawa Y, Kikkawa T, Osumi N. Asymmetric inheritance of Cyclin D2 maintains proliferative neural stem/progenitor cells: a critical event in brain development and evolution. (medlineplus.gov)
  • Cyclin D2 helps to regulate a step in the cycle called the G1-S transition, in which the cell moves from the G1 phase, when cell growth occurs, to the S phase, when the cell's DNA is copied (replicated) in preparation for cell division. (medlineplus.gov)
  • The Cdk- G1/S cyclin complex begins to induce the initial processes of DNA replication, primarily by arresting systems that prevent S phase Cdk activity in G1. (wikipedia.org)
  • Cyclins" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
  • In contrast, Dox treatment was found to induced cyclin B1 accumulation as a result of stimulating its synthesis and inhibiting its degradation. (aspetjournals.org)
  • 2003 Cyclin A2f/f mice were viable and phenotypically normal (data not shown) consistent with our expectation that this "floxed" cyclin A2 allele is usually functionally wild-type. (immune-source.com)
  • Fibroblasts To rule out the possible contribution from cyclin A1 we crossed cyclin A2f/f mice with cyclin A1-null animals (Liu et al. (immune-source.com)
  • 2005 and generated cyclin A1-/-A2f/f mice. (immune-source.com)
  • A subset of cyclins may also function as transcriptional regulators. (umassmed.edu)
  • Downregulation of miR-4755-5p promotes fluoride-induced osteoblast activation via tageting Cyclin D1. (fluoridealert.org)
  • Cyclin D1 E3p5s Xp Rabbit Mab, supplied by Cell Signaling Technology Inc, used in various techniques. (bioz.com)