ViraQuest Inc. , Uncategorized , Estrogen receptor ? causes a G2 cell cycle arrest by inhibiting CDK1 activity through the regulation of cyclin B1, GADD45A, and BTG2 ...
10 products from 6 suppliers. Compare and order Cyclin B1 ELISA Kits. View citations, images, detection ranges, sensitivity, prices and more. Recommended products for the most popular species. Our scientists will help you find the right ELISA kit for your needs.
Wee1 acts as a negative regulator of entry into mitosis (G2 to M transition) by protecting the nucleus from cytoplasmically activated cyclin B1-complexed CDK1 before the onset of mitosis. The activity of wee1 increases during the S and G2 phases, and decreases in M phase when it is hyperphosphorylated. A correlated decrease in wee1 protein level occurs at M/G1 phase, probably due to its degradation. Wee1 specifically phosphorylates and inactivates cyclin B1-complexed CDK1 reaching a maximum during G2 phase and a minimum as cells enter M phase. The phosphorylation of cyclin B1-CDK1 occurs exclusively on Tyr-15 and phosphorylation of monomeric CDK1 does not occur ...
CCNB2 Human Recombinant produced E. coli is a single polypeptide chain containing 422 amino acids (1-398) and having a molecular mass of 47.9 kDa.
Complete information for CCNB2 gene (Protein Coding), Cyclin B2, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
NU6102, CDK1/cyclin B and CDK2/cyclin A3 inhibitor (CAS 444722-95-6), with |98% purity. Join researchers using our high quality biochemicals.
We investigated the occurrence of transcription during mitosis on an RNA pol II‐transcribed gene. We have found that the human cyclin B1 gene is actively transcribed at the mitotic stage. This result is surprising, since it is widely accepted that transcription is repressed during mitosis in higher eukaryotes. Interestingly, in fission yeast the rate of RNA synthesis is maintained during passage through mitosis (Baum et al., 1998). In mammalian cells, until now, no RNA pol II‐dependent transcription has been reported in mitotic cells, although there is evidence showing that 10-20% of the TFIID population remains associated with the condensed mitotic chromatin (Segil et al., 1996). Whether the transcription of the cyclin B1 gene occurs during all the four mitosis phases remains to be elucidated. The cyclin B1 protein is quickly degraded at the metaphase. Whenever a spindle checkpoint is imposed during metaphase, there is a reappearance of cyclin B1 protein due to a loss of cyclin B1 ...
Cyclin B1 (G2- & M-phase Cyclin) Antibody - Without BSA and Azide, Mouse Monoclonal Antibody [Clone V92.1 ] validated in IF, FC, IP (AH10827-100), Abgent
Manni I., Tunici P., Cirenei N., Albarosa R., Colombo B.M., Roz L., Sacchi A., Piaggio G., Finocchiaro G.. Mxi1 is a Mad family member that plays a role in cell proliferation and differentiation. To test the role of Mxi1 on tumorigenesis of glioma cells we transfected a CMV-driven MXI1 cDNA in U87 human glioblastoma cells. Two clones were isolated expressing MXI1 levels 18- and 3.5-fold higher than wild-type U87 cells (clone U87.Mxi1.14 and U87.Mxi1.22, respectively). In vivo, U87.Mxi1.14 cells were not tumorigenic in nude mice and delayed development of tumours was observed with U87.Mxi1.22 cells. In vitro, the proliferation rate was partially and strongly inhibited in U87.Mxi1.22 and U87.Mxi1.14 cells respectively. The cell cycle analysis revealed a relevant accumulation of U87.Mxi1.14 cells in the G(2)/M phase. Interestingly, the expression of cyclin B1 was inhibited to about 60% in U87.Mxi1.14 cells. This inhibition occurs at the transcriptional level and depends, at least in part, on the ...
Metafase di anafase transizione viene attivato attraverso la promozione anafase-complesso (APC / C)-dipendente ubiquitinazione e la...
Cell Cycle, Genes, Tumor, Cell Cycle Genes, Human, Repression, Gene, Dream, Proteins, Regulation, Cell, Cyclin, Cyclin B2, Elements, Mitosis, DNA, Family, Transcription Factors, Apoptosis, DNA Damage
Dominik Schnerch is the author of this article in the Journal of Visualized Experiments: Studieren Proteolyse von Cyclin B an der Single Cell Level in Whole Cell Populationen
amp;amp;amp;amp;amp;amp;amp;amp;lt;div><img src="https://mc.yandex.ru/watch/35930735" style="position:absolute; left:-9999px;" alt="" /></div&gt ...
Fertilization of metaphase II-arrested mouse eggs results in resumption of meiosis and a decrease in both cdc2/cyclin B kinase and MAP kinase activities; the decrease in cdc2/cyclin B kinase activity precedes the decrease in MAP kinase activity. Cycloheximide treatment of metaphase II-arrested mouse eggs also results in resumption of meiosis but bypasses the fertilization-induced Ca2+ transient. However, it is not known if cycloheximide treatment results in the same temporal changes in cdc2/cyclin B kinase and MAP kinase activities that are intimately associated with resumption of meiosis. We report that cycloheximide-treated mouse eggs manifest similar temporal changes in the decrease in both cdc2/cyclin B kinase and MAP kinase activities that occur following fertilization, although cortical granule exocytosis is not stimulated. The decrease in cdc2/cyclin B kinase activity, however, does not seem to be required for the decrease in MAP kinase activity, since the decrease in MAP kinase activity ...
Activation of the Cyclin B/Cdc2 kinase complex triggers entry into mitosis in all eukaryotic cells. Cyclin B1 localization changes dramatically during the cell cycle, precipitously transiting from the cytoplasm to the nucleus at the beginning of mitosis. Presumably, this relocalization promotes the phosphorylation of nuclear targets critical for chromatin condensation and nuclear envelope breakdown. 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. We propose that the observed cytoplasmic localization of Cyclin B1 during interphase reflects the equilibrium between ongoing nuclear import and rapid CRM1-mediated export. In support of this hypothesis, we found that treatment of cells with leptomycin B, which ...
When the APC complex was inhibited by siRNA of APC3, the level of BubR1 remained constant for 60 min after nocodazole release in the presence of CHX, whereas it declined in control cells (Figure 8B). This result was corroborated by the finding from live‐cell assay for proteolysis that depleting APC3 expression abrogated the degradation of BubR1, and concomitantly cells did not enter anaphase for more than 5 h (Supplementary Figure 12 and Supplementary movie 7). When we compared the timing of BubR1 degradation with the degradation of other players in mitosis, such as Cdc20, Cyclin B, Plk1, and Aurora A, we found that BubR1 degradation began before that of Cyclin B (Supplementary Figure 13).. Next, we tested whether Cdc20 was responsible for BubR1 degradation during mitosis. To prevent the cells from exiting mitosis before the analysis began, HeLa cells were transfected with an expression construct to force moderate expression of Cyclin B. siRNA for GFP, Cdc20, or Cdh1 was simultaneously ...
Sea urchin eggs exhibit a cap-dependent increase in protein synthesis within minutes after fertilization. This rise in protein synthesis occurs at a constant rate for a great number of proteins translated from the different available mRNAs. Surprisingly, we found that cyclin B, a major cell-cycle regulator, follows a synthesis pattern that is distinct from the global protein population, so we developed a mathematical model to analyze this dissimilarity in biosynthesis kinetic patterns. The model includes two pathways for cyclin B mRNA entry into the translational machinery: one from immediately available mRNA (mRNAcyclinB) and one from mRNA activated solely after fertilization (XXmRNAcyclinB). Two coefficients, α and β, were added to fit the measured scales of global protein and cyclin B synthesis, respectively. The model was simplified to identify the synthesis parameters and to allow its simulation. The calculated parameters for activation of the specific cyclin B synthesis pathway after
The aim of this thesis was to investigate the prognostic role of the proliferation markers cyclin B1 and Phosphorylated Histone 3 (PPH3) in breast cancer (BC).. In paper I we used an experimental study design, we compared women dying early from their BC with women free from relapse more than eight years after initial diagnosis. All women had stage I, node-negative and hormone receptor positive disease. None had received adjuvant chemotherapy. We found that low-risk node negative patients with high expression of cyclin B1 had a significantly worse outcome than patients with low expression of cyclin B1.. In paper II a population-based case control study was performed to further investigate the prognostic value of cyclin B1. One hundred and ninety women who died from BC were defined as cases and 190 women alive at the time for the corresponding cases death were defined as controls. Inclusion criteria were tumor size 50 mm, no lymph node metastases, and no adjuvant chemotherapy. Two investigators ...
For example, in frogs, cyclin dependent protein kinase 2 (CDK2) binds to cyclin B to form an active kinase which phosphorylates a prereplication complex initiating S phase and mitosis. Cyclin B, a 45Kd protein, accumulates to high levels just before S phase. Its concentration drops sharply at the end of mitosis. The kinase, a 34 Kd protein, is encoded by the CDC2 gene (for cell division cycle gene). A homologous gene exists in humans - the CDK2 gene (cyclin dependent kinase 2) - and controls entry in S phase. These kinases can be considered heterodimers with a kinase catalytic subunit and a cyclin regulatory subunit. In animal cells, there are at least ten different cyclins (A, B, .....) and at least eight different cyclin-dependent kinases (CDK1-8). Another Look at Neurotransmission and Ion Channels. You may have noticed above that some signaling molecules, whose effects are regulated by kinases (b-adrenergic and some olfactory signals by PKA and acetylcholine by PKC for example), are ...
Separase löst alle eukaryotischen Anaphasen aus, indem sie kohäsionsvermittelndes Cohesin spaltet. Bis dahin wird diese essentielle Protease durch Securin inhibiert. Separase kann alternativ durch Assoziation mit Cdk1-Cyclin B1 gehemmt werden, aber der entsprechende Komplex ist in der frühen Mitose wenig abundant und kann nicht erklären, warum Securin in Vertebraten entbehrlich ist. Die Proteinphosphatase 2A (PP2A) bindet Separase ebenfalls, aber die physiologische Rolle dieser Interaktion bleibt rätselhaft. Durch die Inaktivierung des spindle assembly checkpoint (SAC) in der Metaphase kann die Ubiquitin-Ligase APC/C die proteasomale Zerstörung von Securin (und Cyclin B1) vermitteln und dadurch Separase aktivieren. Obwohl sie strukturell mit Caspasen verwandt ist, wurde Separase bisher nicht mit der Apoptose in Verbindung gebracht. Stattdessen wurde in zwei Studien eine Rolle der Hefe-Separase bei der Reparatur von DNS-Schäden vorgeschlagen. Die Frage, ob diese nichtkanonische ...
近 几年我们针对癌细胞中的标靶基因survivin及securin等,进行深入的研究。例如多种人类癌细胞(包括肺癌、乳癌、大肠癌及子宫颈癌等)会大量 表达survivin蛋白,但在正常成人细胞不会表达survivin。Survivin蛋白具有抗细胞凋亡及促细胞分裂的功能,调控癌细胞中 survivin蛋白的表达,与癌症的发生有密切的关系,而抑制survivin蛋白的表达,也可能应用于治疗癌症。我们建立了cyclin B1/cdc2与p38 MAP kinase可分别为正调控及负调控survivin基因及蛋白的表现(Chao et al., 2004, JBC)。此外,利用共轭焦显微镜及免疫萤光染色,建立survivin蛋白会大量表达于癌细胞之有丝分裂期,并会聚集于细胞质分裂期的midbody位 置(Kuo et al., 2004, JBC)。同时我们发现将survivin基因阻断,会促进抗癌药物抑制癌细胞的生长及促细胞凋亡之作用(Chao and Liu, 2006, Mol. ...
Data Availability StatementAll data analyzed or generated through the present research are one of them published content. the thickness from the pulmonary arterial tunica mass media in the model group had been 58.342.01 mmHg, 0.640.046 and 65.33.3%, respectively, that have been higher in comparison to 23 significantly.301.14 mmHg, 0.320.028 and 16.21.3% in the control group, respectively purchase Rocilinostat (P 0.01). The mean pulmonary artery pressure, correct ventricular hypertrophy thickness and index from the pulmonary arterial tunica media in the PTX group had been 42.351.53 mmHg, 0.440.029 and 40.52.6%, respectively, that have been significantly lower in comparison to the model group (P 0.01). Weighed against the control group, the appearance degrees of Ki67 and cyclin B1 in the model group had been considerably elevated (P 0.01), while p27Kip1 appearance was significantly reduced (P 0.01). Pursuing PTX involvement, the appearance degrees of Ki67 and cyclin B1 had been considerably ...
Rabbit polyclonal antibody raised against synthetic phosphopeptide of CCNB1. Synthetic phosphopeptide corresponding to residues surrounding S147 of human CCNB1. (PAB25912) - Products - Abnova
The cyclin E oncogene activates CDK2 to drive cells from G1 to S phase of the cell cycle to commence DNA replication. It coordinates essential cellular functions with the cell cycle including histone biogenesis, splicing, centrosome duplication and origin firing for DNA replication. The two E-cyclins, E1 and E2, are assumed to act interchangeably in these functions. However recent reports have identified unique functions for cyclins E1 and E2 in different tissues, and particularly in breast cancer. Cyclins E1 and E2 localise to distinct foci in breast cancer cells as well as co-localising within the cell. Both E-cyclins are found in complex with CDK2, at centrosomes and with the splicing machinery in nuclear speckles. However cyclin E2 uniquely co-localises with NPAT, the main activator of cell-cycle regulated histone transcription. Increased cyclin E2, but not cyclin E1, expression is associated with high expression of replication-dependent histones in breast cancers. The preferential localisation of
TY - JOUR. T1 - Hydrogen peroxide induces Sp1 methylation and thereby suppresses cyclin B1 via recruitment of Suv39H1 and HDAC1 in cancer cells. AU - Chuang, Jian Ying. AU - Chang, Wen Chang. AU - Hung, Jan Jong. PY - 2011/12/15. Y1 - 2011/12/15. N2 - Sp1 is an important transcription factor for a number of genes that regulate cell growth and survival. Sp1 is an anchor protein that recruits other factors to regulate its target genes positively or negatively, but the mechanism of its functional switch by which positive or negative coregulators are recruited is not clear. In this study, we found that Sp1 could be methylated and that methylation was maintained by treatment with pargyline, a lysine-specific demethylase 1 (LSD1) inhibitor or knock LSD1 down directly. Hydrogen peroxide treatment increased the methylation of Sp1 and repressed Sp1 transcriptional activity. Investigation of the mechanism by which methylation decreased Sp1 activity found that methylation of Sp1 increased the recruitment ...
The key conceptual move, as a biology student, is to be able to see how this system enables the cell (which of course doesnt have any consciousness or intention) to control its passage through the cell cycle every time it needs to divide. A new daughter cell will have very low cyclin levels, which includes the level of the cyclin weve been focused on, cyclin B. As the cell grows and it moves through G1, S, and G2, its level of cyclin B will rise. At a certain concentration of cyclin B, enough MPF is formed to enable to cell to enter M phase. But just at the same moment that the machinery for mitosis and cytokinesis is put into place, cyclin disintegrates. As a result, when the new daughter cells begin their independent existence, cyclin levels are once again very low…setting the stage for another cell cycle.. Note that in addition to these internal signals, external signals also influence cell division. For example, PDGF (platelet derived growth factor) stimulates a variety of cells to ...
Ccnb1ip1 - mouse gene knockout kit via CRISPR, 1 kit. |dl||dt|Kit Component:|/dt||dd|- |strong|KN302805G1|/strong|, Ccnb1ip1 gRNA vector 1 in |a href=http://www.origene.com/CRISPR-CAS9/Detail.
Ribociclib D6 (LEE011 D6) is a deuterium labeled Ribociclib. Ribociclib is a highly specific CDK4/6 inhibitor with IC50 values of 10 nM and 39 nM, respectively, and is over 1,000-fold less potent against the cyclin B/CDK1 complex. - Mechanism of Action & Protocol.
臺大位居世界頂尖大學之列,為永久珍藏及向國際展現本校豐碩的研究成果及學術能量,圖書館整合機構典藏(NTUR)與學術庫(AH)不同功能平台,成為臺大學術典藏NTU scholars。期能整合研究能量、促進交流合作、保存學術產出、推廣研究成果。. To permanently archive and promote researcher profiles and scholarly works, Library integrates the services of "NTU Repository" with "Academic Hub" to form NTU Scholars.. ...
The activation of the ubiquitin ligase APC/C requires the phosphorylation of multiple subunits. Because depletion or inactivation of the Xenopus Polo-like kinase 1 (Plx1) in meiotically arrested egg extracts blocks APC/C-dependent degradation of cyclin B ( 5), many investigators have tried to directly link the activities of Plk1 and APC/C. Although Plk1 is able to phosphorylate subunits of the APC/C in vitro, this phosphorylation contributes only marginally to its activation ( 6). In contrast, cyclin B/Cdk1 seems to have a major role in the phosphorylation and activation of the APC/C, thereby triggering its own inactivation at the end of mitosis ( 7).. Although Plk1 can contribute synergistically to the cyclin B/Cdk1-mediated activation of the APC/C ( 6), this observation is not sufficient to explain the crucial role of Plk1/Plx1 in the activation of the APC/C. Intriguing insights have come from studies of the cytostatic factor (CSF) in Xenopus oocytes, where CSF activity prevents parthogenetic ...
To determine whether Trim39 could inhibit the APC/C, we added either maltose-binding protein (MBP) or MBP-Trim39 protein to lysates prepared from HeLa cells that had been synchronized in nocodazole and then released (by washout of the nocodazole). As shown in Fig. 1 C, cyclin B1 was quickly degraded in the presence of recombinant MBP protein as these lysates exited from the mitotic arrest, whereas degradation of endogenous cyclin B1 was nearly abolished by addition of recombinant MBP-Trim39. This inhibition was not observed using the C44A mutant, suggesting that E3 ubiquitin ligase activity is required for APC/C inhibition (Fig. 1 C). Indeed, cyclin B1 was more rapidly degraded in the presence of the catalytically inactive Trim39 mutant, suggesting that this protein might interfere with the functioning of the endogenous protein. To confirm a direct role for Trim39 in APC/C inhibition, we incubated APC/C immunoprecipitated from HeLa cells with MBP or MBP-Trim39, E1, E2, ubiquitin, and ...
We show that in fission yeast the mitotic B type cyclin Cdc13/Cdc2 kinase associates with replication origins in vivo. This association is dependent on the origin recognition complex (ORC), is established as chromosomes are replicated, and is maintained during G2 and early mitosis. Cells expressing …
The effect was found to be associated with increased expression of E2F-1 in cervical cancer cells as there is no CAPE-mediated induction of E2F-1 in the precancerous cervical Z172 cells. CAPE also upregulated the E2F-1 target genes cyclin A, cyclin E, and apoptotic protease activation of factor 1 (Apaf-1) but down regulated cyclin B and myeloid leukemia cell differentiation protein (Mcl-1). These results suggested the involvement of E2F-1 in CAPE-mediated growth inhibition and cell cycle arrest. Transient transfection studies with luciferase reporters revealed that CAPE altered transcriptional activity of the apaf-1 and mcl-1 promoters. Further studies using chromatin immunoprecipitation (ChIP) assays demonstrated that in CAPE-treated cells, E2F-1 binding to the apaf-1 and cyclin B promoters was increased and decreased, respectively. Furthermore, E2F-1 silencing abolished CAPE-mediated effects on cell cycle arrest, apoptosis, and related gene expression ...
We report the isolation of UME3, a C‐type cyclin that is required for the full repression of several early meiotic genes (e.g. SPO13) and SSA1, a member of the HSP70 superfamily. Similarly to other cyclin C family members, UME3 mRNA and protein levels remained unchanged throughout the mitotic cell cycle. However, under conditions that induce SSA1 or SPO13 transcription, we demonstrate that Ume3p is subjected to degradation. This destruction is required for normal meiotic gene induction, as a mutation that stabilizes Ume3p resulted in a 2‐fold reduction in SPO13 mRNA accumulation. These findings reveal the first observed regulation of a C‐type cyclin. Moreover, the destruction of Ume3p in response to heat shock or developmental cues represents a new set of regulatory signals by which any cyclin is controlled. We identified three cis‐acting domains (PEST‐rich, RXXL and the cyclin box) that contribute to the destruction of Ume3p during heat shock. In cultures exposed to heat shock, Ume3p ...
Around 10.000 - 150.000 endogenous DNA damage-induced lesions occur in a human body per day and cell. Accumulation of unrepaired lesions can lead to aneuploidy and the loss of genomic integrity which in turn contributes to tumor formation. Therefore, an efficient DNA damage response has to be initiated, in the end leading to cell cycle inhibition and induction of repair. Since it is known that a recently characterized human multiprotein complex named LINC (or human dREAM) together with B-MYB is involved in the regulation of G2/M gene expression (Plk1, cyclin B1, cdc2 etc.), its function in the DNA damage response was analyzed in this study. In growing cells B-MYB is associated to the LIN core complex which consists of 5 different proteins named LIN-9, LIN-54, LIN-52, LIN-37 and RbAp48. After induction of DNA damage B-MYB leaves the complex and binding of E2F4 and p130 to LINC is induced. Importantly, the upstream pathway leading to LINC rearrangement is dependent on the activation of p53 and ...
Natural borneol (NB) has been used as a promoter of drug absorption and widely used in candies, beverages, baked goods, chewing gum and other foods. Thus, we investigated whether NB could potentiate the cellular uptake of BDCur, and elucidated the molecular mechanisms of their combined inhibitory effects on HepG2 cells. Our results demonstrate that NB significantly enhanced the cellular uptake of BDCur. Induction of cell cycle arrest in HepG2 cells by NB and BDCur in combination was evidenced by accumulation of the G2/M cell population. Further investigation on the molecular mechanism showed that NB and BDCur in combination resulted in a significant decrease in the expression level of Cdc2 and cyclin B ...
Sigma-Aldrich offers abstracts and full-text articles by [Eunju Kim, Se-Jin Yoon, Eun-Young Kim, Yunna Kim, Hyun-Seo Lee, Kyeoung-Hwa Kim, Kyung-Ah Lee].
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Breast cancer is one of the most common malignancies in women. Due to early detection and the use of screening programs approximately 60% of all new cases lack lymph node involvement. Today, a substantial proportion of these women will be offered adjuvant systemic chemotherapy. However, better proliferation markers are needed to predict patient outcome and to avoid overtreatment. Cyclin A, cyclin E and Ki-67 are all markers for proliferation and involved in the regulation of the cell cycle. Overexpression has been associated with disease recurrence in several studies, but the results have not been consistent. However, none of these studies has investigated aberrant expression of cyclin E (the expression of cyclin E during phases of the cell cycle other than late G1 and early S-phase). Studies have shown that aberrant cyclin E might provide additional prognostic information compared to cyclin E alone.. The aims of this thesis were 1.to investigate the prognostic value of cyclin A, cyclin E and ...
Our experiments demonstrate the existence of a complex containing both cyclin E and several components of the U2 snRNP in vivo, in particular SAP 155, SAP 145, and SAP 114. We were able to detect the association between both cyclin E and SAP 155, as well as cdk2 and SAP 155, through either of the components in cellular lysates. The cyclin E-SAP 155 association can also be shown in the yeast two-hybrid system and can be reconstituted in vitro by using recombinant components. Furthermore, we found that cyclin E-specific antibodies were able to precipitate U1 and U2 snRNAs, as well as the pre-mRNA substrate from preassembled spliceosomes.. We find that one component of U2 snRNP, SAP 155, serves as an excellent substrate for cyclin E-cdk2 both in the U2/E/k2 complex precipitated from cells and as a recombinant protein in vitro. Phosphorylation of SAP 155 in the U2/E/k2 complex can be inhibited by preincubation of these complexes with p21, a known cyclin-kinase inhibitor. Taken together, these data ...
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マウス・モノクローナル抗体 ab38 交差種: Ms,Rat,Hu 適用: WB,IP,IHC-P,IHC-Fr,Flow Cyt…Cyclin A2抗体一覧…画像、プロトコール、文献などWeb上の情報が満載のアブカムの Antibody…
Dalby, B. and Glover, D. M. (1993). Discrete sequence elements control posterior pole accumulation and translational repression of maternal cyclin B RNA in Drosophila. EMBO J 12: 1219-27 DAngiolella, V., et al. (2001). Role for cyclin-dependent kinase 2 in mitosis exit. Curr. Bio. 11: 1221-1226. 11516956 de Moor, C. H. and Richter, J. D. (1999). Cytoplasmic polyadenylation elements mediate masking and unmasking of cyclin B1 mRNA. EMBO J. 18(8): 2294-2303 Detweiler, C. S. and Li, J. J. (1998). Ectopic induction of Clb2 in early G1 phase is sufficient to block prereplicative complex formation in Saccharomyces cerevisiae. Proc. Natl. Acad. Sci. 95(5): 2384-9 Dawson, I. A., Roth, S. and Artavanis-Tsakonas, S. (1995). The Drosophila cell cycle gene fizzy is required for normal degradation of cyclins A and B during mitosis and has homology to the CDC20 gene of Saccharomyces cerevisiae. J Cell Biol 129: 725-737 Dulic, V., et al. (1998). Nuclear accumulation of p21Cip1 at the onset of mitosis: a role ...
The representation of cyclins and cyclin-dependent kinases (cdks) was analyzed during progressive development of the bone cell phenotype in cultures of normal diploid rat calvarial osteoblasts. Three developmental stages were examined: (a) proliferation; (b) monolayer confluency; and (c) mineralization of the bone extracellular matrix. We demonstrate that the presence of cyclins and cdks is not restricted to the proliferation period. Consistent with their role in cell cycle progression, cdc2 and cdk2 decrease postproliferatively. However, cdk4 and cyclins A, B, and D1 persist in confluent cells. Cyclin E is significantly up-regulated during the extracellular matrix mineralization developmental period. Examination of the cytoplasmic levels of these cell cycle regulatory proteins indicates a marked increase in cyclin B in the late differentiation stage. The elevation of nuclear cyclin E and cytoplasmic cyclin B is not observed in osteoblasts maintained under culture conditions that do not support
Methods and results: Levels of FOXM1 and its targets were determined by immunoprecipitation and real-time PCR analyses in rat and human samples. FOXM1 function was investigated by either FOXM1 silencing or overexpression in human HCC cell lines. Activation of FOXM1 and its targets (Aurora Kinose A, Cdc2, cyclin B1, Nek2) occurred earlier and was most pronounced in liver lesions from F344 than BN rats, leading to the highest number of Cdc2-cyclin B1 complexes (implying the highest G2-M transition) in F344 rats. In human HCC, the level of FOXM1 progressively increased from surrounding non-tumorous livers to HCC, reaching the highest levels in tumours with poorer prognosis (as defined by patients length of survival). Furthermore, expression levels of FOXM1 directly correlated with the proliferation index, genomic instability rate and microvessel density, and inversely with apoptosis. FOXM1 upregulation was due to extracellular signal-regulated kinase (ERK) and glioblastoma-associated oncogene 1 ...
Entry into mitosis in Aspergillus nidulans is regulated by the coordinate function of two serine/threonine protein kinases, NIMXCDC2 and NIMA. NIMXCDC2 is an essential histone H1 kinase that is structurally and functionally homologous to fission yeast p34cdc2 (Osmani et al., 1994). NIMA is a β-casein kinase and is structurally distinct from p34cdc2, containing an amino-terminal catalytic domain and a carboxyl-terminal regulatory domain (Osmani et al., 1988b; Lu et al., 1993; Pu and Osmani, 1995; Pu et al., 1995). Failure to properly activate either of these kinases in G2 prevents the initiation of mitosis, and the combined action of both kinases is critical for coordinating changes in chromosome, microtubule, and nuclear membrane structure during mitosis. For example, mutations preventing the activation of NIMXCDC2 in G2 normally arrests cells in late G2 (Osmani et al., 1991a; 1994). Although overexpression of NIMA can overcome this interphase arrest, the ensuing mitosis is disorganized such ...
DAT-230 is a promising microtubule inhibitor that has great potential for the treatment of fibrosarcoma in vitro and in vivo. DAT-230 exhibited potent anti-proliferative activity against various cancer cells. DAT-230 -treatment in HT-1080 cells resulted in microtubule de-polymerization and G2/M phase arrest preceding apoptosis. Phosphor-cdc2 (thr14/tyr15) reduction, cyclin B1 accumulation and aberrant spindles denoted the cyclin B1-cdc2 complex active and M phase arrest in HT-1080 cells treated with DAT-230. Apoptosis induced by DAT-230 was related with the activation of caspase-9, caspase-3 and PARP cleavage, which were at the downstream of mitochondria.
In humans, there are two A-type cyclins - an embryonic-specific cyclin A1 and a somatic cyclin A2. Cyclin A1 is only expressed in meiosis and very early embryos, whereas cyclin A2 is present in proliferating somatic cells