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anti-Human CDC25B Anticorps:
anti-Mouse (Murine) CDC25B Anticorps:
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Human Polyclonal CDC25B Primary Antibody pour IHC (p), WB - ABIN537582
Wu, Slomovitz, Celestino, Chung, Thornton, Lu: Coordinate expression of Cdc25B and ER-alpha is frequent in low-grade endometrioid endometrial carcinoma but uncommon in high-grade endometrioid and nonendometrioid carcinomas. dans Cancer research 2003
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Human Polyclonal CDC25B Primary Antibody pour IHC (fro), ELISA - ABIN543791
Ito, Yoshida, Matsuzuka, Matsuura, Nakamura, Nakamine, Kakudo, Kuma, Miyauchi: Cdc25A and cdc25B expression in malignant lymphoma of the thyroid: correlation with histological subtypes and cell proliferation. dans International journal of molecular medicine 2004
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Human Polyclonal CDC25B Primary Antibody pour WB - ABIN6677874
Wang, Wang, Mei, Yin, Geng, Zhang, Wu, Lin: The BET bromodomain inhibitor JQ1 radiosensitizes non-small cell lung cancer cells by upregulating p21. dans Cancer letters 2017
Mouse (Murine) Polyclonal CDC25B Primary Antibody pour WB - ABIN871399
Li, Park, Liang, Zhao: Cell cycle G2/M arrest through an S phase-dependent mechanism by HIV-1 viral protein R. dans Retrovirology 2010
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Increased expression of CDC25B or CDC25C are mechanisms by which skin cancers evade apoptotic cell death.
Depletion of TIAR accelerates mitotic entry and leads to chromosomal instability in response to replication stress, in a manner that can be alleviated by the concomitant depletion of Cdc25B or inhibition of CDK1. Since TIAR retains CDK1 in GMGs and attenuates CDK1 activity, we propose that the assembly of GMGs may represent a so far unrecognized mechanism that contributes to the activation of the G2/M checkpoint
These findings indicate that CDC25B facilitates the dephosphorylation of nucleoprotein (NP), which is vital for regulating NP functions and the life cycle of influenza a virus.
miR-152 was a tumor suppressor in EC that inhibited proliferation of human endometrial cancer cells via inducing G2/M phase arrest by suppressing CDC25B expression.
High CDC25B expression is associated with non-small cell lung cancer metastasis.
YWHAE silencing induces cell proliferation, invasion and migration through the up-regulation of CDC25B and MYC in gastric cancer cells.
our study demonstrate that KCTD12 binds to CDC25B and activates CDK1 and Aurora A to facilitate the G2/M transition and promote tumorigenesis and that Aurora A phosphorylates KCTD12 at serine 243 to trigger a positive feedback loop, thereby potentiating the effects of KCTD12. Thus, the KCTD12-CDC25B-CDK1-Aurora A axis has important implications for cancer diagnoses and prognoses.
While the low expression level of DUSP7 was restricted to patients with positive rheumatoid factor and anti-citrullinated protein antibodies, the altered expression of CDC25B correlated with the activity of early arthritis.
Conformational flexibility of the complete catalytic domain of Cdc25B phosphatase has been demonstrated.
Data indicate that nine compounds were identified with Ki values for CDC25A, -B and -C ranging from 0.01 to 4.4 muM.
High CDC25B expression is associated with esophageal carcinoma.
Solution NMR studies reveal no global flexibility in the structure of CDC25b catalytic domain
For the first time, we demonstrate that miRNA-211 is a direct negative regulator of CDC25B expression in TNBC cells, alters other related target proteins CCNB1 and FOXM1, and then inhibits breast cancer cells growth, migration, and invasion
FK-3000 exerts its antiproliferative effect through G2/M cell cycle arrest via downregulation of cyclin B and phospho-CDC2 by p38 MAPK phosphorylation and CDC25B dephosphorylation .
Our results suggest that expression of CDC25B may be used as a potential prognostic marker in the pathogenesis of retinoblastoma.
RSK promotes G2/M transition in mammalian cells through activating phosphorylation of Cdc25A and Cdc25B.
Cdc25B upregulation and 14-3-3sigma downregulation might promote development of bladder cancer and suggested a poor prognosis.
Positive expression of CDC25B in astrocytoma affects the prognosis in an adverse manner.
CDC25B is a pro-influenza A virus host factor.
CDC25B, through activation of a centrosomal pool of CDK2, stabilises the local pool of Mps1 which in turn regulates the level of centrin 2 at the centrosome.
CDC25B is required for efficient neuron production in vertebrates.
data suggest an important role of CDC25B for microtubule nucleation and organization. N-terminal of CDC25B is required for regulating the microtubule dynamics and mitotic function.
LSD1 is essential for oocyte meiotic progression by upregulating CDC25B expression.
The role of Cdc25c and Cdc25b in activating G2/M cell cycle checkpoint in zygote.
AURKA induced phosphorylation and recruitment of CDC25B to MTOCs prior to p-Cyclin B1-Ser123, and this sequential regulation is essential for the commitment of the oocytes to resume meiosis.
Data indicate that 14-3-3epsilon is required for the mitotic entry in the fertilized mouse eggs and responsible for sequestering the CDC25B in cytoplasm. Its binding to CDC25B-S321 phosphorylated by PKA induces mitotic arrest.
contributes to metaphase arrest in mouse oocytes
Ser321 of Cdc25B is the specific binding site for 14-3-3epsilon binding.
Protein kinase A the early development of mouse embryos by phosphorylation of S149 and S321 of CDC25B, which plays an important role in the regulation of G(2)/M transition in the mitotic cell cycle of fertilized mouse eggs.
In the DNA damage response, instead of inhibiting cyclin B-CDK1 through destruction of Cdc25A phosphatase, oocytes utilize an inhibitory phosphorylation of Cdc25B.
Cdc25B overexpression in early mouse two-cell embryos reverses two-cell block and promotes their development into four-cell stage by activating MPF.
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.
CDC25A and CDC25B but not CDC25C compensate for each other to maintain the proliferative capacity of intestinal epithelial stem and progenitor cells
Ser(149) may be another potential PKA phosphorylation target of Cdc25B in G(2)/M transition of fertilized mouse eggs and Cdc25B as a direct downstream substrate of PKA in mammals
Cdc25b phosphatase is required for resumption of meiosis during oocyte maturation
Cdc25A, or possibly other phosphatases, is able to functionally compensate for the loss of Cdc25B and Cdc25C in mice
Shh contributes to CDC25B transcriptional activation in the neural tube both of chick and mouse embryos
Cdc25b is regulated by Foxm1 during heart development.
p38 regulates the timing of mitotic entry via modulation of Cdc25B activity under normal nonstress conditions
Data show that the expression of cell cycle genes, Cdc25b, in the optic nerves is downregulated in a conditional ablation of Shh mutant mice.
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.
cell division cycle 25 homolog B
, cell division cycle 25 homolog B (S. pombe)
, M-phase inducer phosphatase 2-like
, m-phase inducer phosphatase 2-like
, cell division cycle 25B
, M-phase inducer phosphatase 2
, dual specificity phosphatase Cdc25B