cdc25 phosphatases


Summary: A subclass of dual specificity phosphatases that play a role in the progression of the CELL CYCLE. They dephosphorylate and activate CYCLIN-DEPENDENT KINASES.

Top Publications

  1. Dulic V, Drullinger L, Lees E, Reed S, Stein G. Altered regulation of G1 cyclins in senescent human diploid fibroblasts: accumulation of inactive cyclin E-Cdk2 and cyclin D1-Cdk2 complexes. Proc Natl Acad Sci U S A. 1993;90:11034-8 pubmed
  2. Bouldin C, Kimelman D. Dual fucci: a new transgenic line for studying the cell cycle from embryos to adults. Zebrafish. 2014;11:182-3 pubmed publisher
  3. Dozier C, Mazzolini L, Cénac C, Froment C, Burlet Schiltz O, Besson A, et al. CyclinD-CDK4/6 complexes phosphorylate CDC25A and regulate its stability. Oncogene. 2017;36:3781-3788 pubmed publisher
    ..Thus our results identify cyclinD-CDK4/6 complexes as novel regulators of CDC25A stability during G1 phase, generating a negative feedback loop allowing control of the G1/S transition. ..
  4. Yuan P, Li J, Zhou F, Huang Q, Zhang J, Guo X, et al. NPAS2 promotes cell survival of hepatocellular carcinoma by transactivating CDC25A. Cell Death Dis. 2017;8:e2704 pubmed publisher
    ..Thereby, NPAS2 may serve as a potential therapeutic target in HCC patients. ..
  5. Rostom S, Badr M, Abd El Razik H, Ashour H. Structure-based development of novel triazoles and related thiazolotriazoles as anticancer agents and Cdc25A/B phosphatase inhibitors. Synthesis, in vitro biological evaluation, molecular docking and in silico ADME-T studies. Eur J Med Chem. 2017;139:263-279 pubmed publisher
  6. Feng M, Yu Q. miR-449 regulates CDK-Rb-E2F1 through an auto-regulatory feedback circuit. Cell Cycle. 2010;9:213-4 pubmed
  7. Cui C, Ren X, Liu D, Deng X, Qin X, Zhao X, et al. 14-3-3 epsilon prevents G2/M transition of fertilized mouse eggs by binding with CDC25B. BMC Dev Biol. 2014;14:33 pubmed publisher
    ..14-3-3? is primarily responsible for sequestering the CDC25B in cytoplasm and 14-3-3? binding to CDC25B-S321 phosphorylated by PKA induces mitotic arrest at one-cell stage by inactivation of MPF in fertilized mouse eggs. ..
  8. Zwergel C, Czepukojc B, Evain Bana E, Xu Z, Stazi G, Mori M, et al. Novel coumarin- and quinolinone-based polycycles as cell division cycle 25-A and -C phosphatases inhibitors induce proliferation arrest and apoptosis in cancer cells. Eur J Med Chem. 2017;134:316-333 pubmed publisher
    ..Compound 2c displayed increased phosphorylation levels of histone H3, induction of PARP and caspase 3 cleavage, highlighting its contribution to cell death through pro-apoptotic effects. ..
  9. Iyirhiaro G, Im D, Boonying W, Callaghan S, During M, Slack R, et al. Cdc25A Is a Critical Mediator of Ischemic Neuronal Death In Vitro and In Vivo. J Neurosci. 2017;37:6729-6740 pubmed publisher
    ..An increase in pRb phosphorylation has been previously linked to ischemic neuronal death. Our results identify Cdc25A as a potential target for neuroprotectant strategy for the treatment of delayed ischemic neuronal death. ..

More Information


  1. Barzegar M, Ma S, Zhang C, Chen X, Gu Y, Shang C, et al. SKLB188 inhibits the growth of head and neck squamous cell carcinoma by suppressing EGFR signalling. Br J Cancer. 2017;117:1154-1163 pubmed publisher
    ..The results provide a basis for further clinical investigation of SKLB188 as a targeted therapy for HNSCC. Our findings may open a new avenue for development of novel EGFR inhibitors for treatment of HNSCC and other cancers. ..
  2. Liu X, Zong W, Li T, Wang Y, Xu X, Zhou Z, et al. The E3 ubiquitin ligase APC/CCdh1 degrades MCPH1 after MCPH1-?TrCP2-Cdc25A-mediated mitotic entry to ensure neurogenesis. EMBO J. 2017;36:3666-3681 pubmed publisher
    ..This study provides a mechanistic understanding of how MCPH1 controls neural stem cell fate and brain development. ..
  3. Sung M, Kawasaki I, Shim Y. Depletion of cdc-25.3, a Caenorhabditis elegans orthologue of cdc25, increases physiological germline apoptosis. FEBS Lett. 2017;591:2131-2146 pubmed publisher
    ..3 mutants is induced by accumulation of DSBs, leading to a loss of PGL-1 and PGL-3 in germ cells, which promotes cytoplasmic translocation of SIR-2.1, and finally activates the core apoptotic machinery. ..