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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 (show CCNB1 Proteins) and FOXM1 (show FOXM1 Proteins), 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 (show CDK1 Proteins) by p38 MAPK (show MAPK14 Proteins) 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 (show RPS6KA1 Proteins) promotes G2/M transition in mammalian cells through activating phosphorylation of Cdc25A (show CDC25A Proteins) 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.
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 (show KDM1A Proteins) is essential for oocyte meiotic progression by upregulating CDC25B expression.
The role of Cdc25c (show CDC25C Proteins) and Cdc25b in activating G2/M cell cycle checkpoint in zygote.
AURKA (show AURKA Proteins) induced phosphorylation and recruitment of CDC25B to MTOCs prior to p-Cyclin B1 (show CCNB1 Proteins)-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.
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 (show CDK1 Proteins) through destruction of Cdc25A (show CDC25A Proteins) 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 (show MSLN Proteins).
MCPH1 (show MCPH1 Proteins), through its function in the Chk1 (show CHEK1 Proteins)-Cdc25 (show CDC25C Proteins)-Cdk1 (show CDK1 Proteins) 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.
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