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Cell division cycle 25 homolog B

CDC25B is a member of the CDC25 family of phosphatases. CDC25B activates the cyclin dependent kinase CDC2 by removing two phosphate groups and it is required for entry into mitosis. CDC25B shuttles between the nucleus and the cytoplasm due to nuclear localization and nuclear export signals. The protein is nuclear in the M and G1 phases of the cell cycle and moves to the cytoplasm during S and G2. CDC25B has oncogenic properties, although its role in tumor formation has not been determined. Multiple transcript variants for this gene exist. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: PCNA, cdc25, CDC2, Cdc25A, CAN
Papers on Cdc25B
Identification of a redox-modulatory interaction between selenoprotein W and 14-3-3 protein.
Kim et al., Seoul, South Korea. In Biochim Biophys Acta, Jan 2016
We have previously reported that the binding of 14-3-3 protein to its target proteins, including CDC25B, Rictor and TAZ, is inhibited by the interaction of 14-3-3 protein with SelW.
Generation of N-Heterocycles via Tandem Reactions of N '-(2-Alkynylbenzylidene)hydrazides.
Wu et al., Jiaxing, China. In Chem Rec, Nov 2015
Biological evaluation suggested that some compounds showed promising activities for inhibition of CDC25B, TC-PTP, HCT-116, and PTP1B.
Differential Protein Expression in Small Intestinal Neuroendocrine Tumors and Liver Metastases.
Itzkowitz et al., New York City, United States. In Pancreas, Nov 2015
The SI-NET liver metastases demonstrated upregulation of P-ERK and p27 but downregulation of CDK2 and CDC25B.
Plumbagin inhibits growth of gliomas in vivo via suppression of FOXM1 expression.
Yu et al., Xuzhou, China. In J Pharmacol Sci, Jul 2015
Importantly, we also determined that the expressions of FOXM1 and its downstream target effectors, including cyclin D1 and Cdc25B, were down-regulated in the treated group, while the expressions of p21 and p27 were increased; the latter findings corroborate the results of our previous in vitro study.
Anti-cancer chalcones: Structural and molecular target perspectives.
Asati et al., Bilāspur, India. In Eur J Med Chem, Jul 2015
Several natural and (semi) synthetic chalcones have shown anti-cancer activity due to their inhibitory potential against various targets namely ABCG2/P-gp/BCRP, 5α-reductase, aromatase, 17-β-hydroxysteroid dehydrogenase, HDAC/Situin-1, proteasome, VEGF, VEGFR-2 kinase, MMP-2/9, JAK/STAT signaling pathways, CDC25B, tubulin, cathepsin-K, topoisomerase-II, Wnt, NF-κB, B-Raf and mTOR etc.
Cell cycle and cell fate in the developing nervous system: the role of CDC25B phosphatase.
Pituello et al., Toulouse, France. In Cell Tissue Res, 2015
Here, we summarize recent data describing how cell cycle dynamics affect the switch between proliferation and differentiation, with an emphasis on the roles played by the cell cycle regulators, the CDC25 phosphatases.
LSD1 is essential for oocyte meiotic progression by regulating CDC25B expression in mice.
Chen et al., United States. In Nat Commun, 2014
Mechanistically, upregulation of CDC25B, a phosphatase that activates CDK1, is responsible for precocious meiotic resumption and also contributes to subsequent spindle and chromosomal defects.
Lats1 suppresses centrosome overduplication by modulating the stability of Cdc25B.
Nojima et al., Suita, Japan. In Sci Rep, 2014
We also found that Lats1 physically interacts with Cdc25B phosphatase that localizes both at the centrosome and in the nucleus and regulates the linkage between the centrosome cycle and mitotic progression.
Biomarkers for predicting the response of esophageal squamous cell carcinoma to neoadjuvant chemoradiation therapy.
Natsugoe et al., Kagoshima, Japan. In Surg Today, 2014
There are seven categories of molecules known to correlate with the response and/or prognosis: tumor suppressors (p53, p21), cell cycle regulators (Cyclin D1, CDC25B, 14-3-3sigma), DNA repair molecules (p53R2, ERCC1), drug resistance proteins [metallothionein (MT)], angiogenic factors (VEGF), molecules involved in cell proliferation/invasion/metastasis (Ki-67, COX-2) and hedgehog signaling molecules (Gli-1).
Therapeutic targeting the cell division cycle 25 (CDC25) phosphatases in human acute myeloid leukemia--the possibility to target several kinases through inhibition of the various CDC25 isoforms.
Bruserud et al., Bergen, Norway. In Molecules, 2013
The cell division cycle 25 (CDC25) phosphatases include CDC25A, CDC25B and CDC25C.
Oocytes progress beyond prophase in the presence of DNA damage.
Carroll et al., London, United Kingdom. In Curr Biol, 2012
In the DNA damage response, instead of inhibiting cyclin B-CDK1 through destruction of Cdc25A phosphatase, oocytes utilize an inhibitory phosphorylation of Cdc25B.
MCPH1 regulates the neuroprogenitor division mode by coupling the centrosomal cycle with mitotic entry through the Chk1-Cdc25 pathway.
Wang et al., Jena, Germany. In Nat Cell Biol, 2011
MCPH1, through its function in the Chk1-Cdc25-Cdk1 pathway to couple the centrosome cycle with mitosis, is required for precise mitotic spindle orientation and thereby regulates the progenitor division mode to maintain brain size.
MicroRNA-148a is down-regulated in human pancreatic ductal adenocarcinomas and regulates cell survival by targeting CDC25B.
Tannapfel et al., Bochum, Germany. In Lab Invest, 2011
We identified CDC25B as novel miR-148a target which may confer a proliferative advantage in pancreatic ductal adenocarcinomas.
Study of the docking-dependent PLK1 phosphorylation of the CDC25B phosphatase.
Bouche et al., Toulouse, France. In Biochem Biophys Res Commun, 2011
there are 13 sites phosphorylated by PLK1 in CDC25B.This study illustrates the complexity of the phosphorylation pattern and of the subsequent regulation of CDC25B activity.
Transcriptional repression of Cdc25B by IER5 inhibits the proliferation of leukemic progenitor cells through NF-YB and p300 in acute myeloid leukemia.
Yamashita et al., Hamamatsu, Japan. In Plos One, 2010
Transcriptional repression mediated by IER5 regulates Cdc25B expression levels via the release of NF-YB and p300 in acute myeloid leukemia.
HIV/gp120 decreases adult neural progenitor cell proliferation via checkpoint kinase-mediated cell-cycle withdrawal and G1 arrest.
Lipton et al., Los Angeles, United States. In Cell Stem Cell, 2007
We demonstrate that HIV/gp120 arrests cell-cycle progression of aNPCs at the G1 phase via a cascade consisting of p38 mitogen-activated protein kinase (MAPK) --> MAPK-activated protein kinase 2 (a cell-cycle checkpoint kinase) --> Cdc25B/C.
p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage.
Yaffe et al., Cambridge, United States. In Cancer Cell, 2007
MK2 depletion in p53-deficient cells, but not in p53 wild-type cells, caused abrogation of the Cdc25A-mediated S phase checkpoint after cisplatin exposure and loss of the Cdc25B-mediated G2/M checkpoint following doxorubicin treatment, resulting in mitotic catastrophe and pronounced regression of murine tumors in vivo.
Centrosome-associated Chk1 prevents premature activation of cyclin-B-Cdk1 kinase.
Lukas et al., Copenhagen, Denmark. In Nat Cell Biol, 2004
Activation of centrosomal Cdk1 in late prophase seemed to be mediated by cytoplasmic Cdc25B, whose activity is controlled by centrosome-associated Chk1.
Dual phosphorylation controls Cdc25 phosphatases and mitotic entry.
Fornace et al., Bethesda, United States. In Nat Cell Biol, 2003
Negative regulation of the Cdc25C protein phosphatase by phosphorylation on Ser 216, the 14-3-3-binding site, is an important regulatory mechanism used by cells to block mitotic entry under normal conditions and after DNA damage.
Initiation of a G2/M checkpoint after ultraviolet radiation requires p38 kinase.
Fornace et al., Bethesda, United States. In Nature, 2001
In vitro, p38 binds and phosphorylates Cdc25B at serines 309 and 361, and Cdc25C at serine 216; phosphorylation of these residues is required for binding to 14-3-3 proteins.
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