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Stat3 (zeige STAT3 Proteine) regulates cell proliferation and axis extension in part via upregulation of Cdc25a expression during oogenesis. Accordingly, restoring Cdc25a expression in stat3 (zeige STAT3 Proteine) mutants partially suppressed cell proliferation and gastrulation defects.
MCPH1 (zeige MCPH1 Proteine) interacts with and promotes the E3 ligase betaTrCP2 to degrade Cdc25A independent of DNA damage. Overexpression of betaTrCP2 or the knockdown of Cdc25A remedies the high mitotic index and rescues the premature differentiation of Mcph1 (zeige MCPH1 Proteine)-deficient neuroprogenitors in vivo MCPH1 (zeige MCPH1 Proteine) itself is degraded by APC (zeige APC Proteine)/CCdh1, but not APC (zeige APC Proteine)/CCdc20, in late mitosis and G1 phase.
The cytoplasmic relocalization of CDC25A in skin cancers results in acquisition of an antiapoptotic function for CDC25A.
NPAS2 has a critical role in HCC cell survival and tumor growth, which is mainly mediated by transcriptional upregulation of CDC25A.
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.
These results identify a new positive regulatory loop between Cdc25A and its CDK-cyclin substrates which contributes to accelerate entry into mitosis through the regulation of Cdc25A activity in G2.
The expression level of Cdc25A was significantly increased (<0.05) after treatment with miR (zeige MLXIP Proteine)-675 mimics.
miR-497 modulates the growth of chondrosarcoma cells by targeting Cdc25A.
This study demonstrated that the cell cycle pathway and the cdc25a gene may be crucial in the pathogenesis and progression of hepatocellular carcinoma.
Increased CDC25A is associated with invasiveness in Non-small Cell Lung Cancer.
Data indicate that nine compounds were identified with Ki values for CDC25A, -B and -C ranging from 0.01 to 4.4 muM.
Our results identify Cdc25A as a potential target for neuroprotectant strategy for the treatment of delayed ischemic neuronal death.
CDC25A-deficient embryonic stem cells resist high doses of ATR inhibitors, which we show is due to their failure to prematurely enter mitosis in response to the drugs.
These results showed that IGF1 regulated the expression of BOULE and CDC25A mRNAs via ERK1/2 signaling and in T-independent pathway during spermatogenesis in the adult mouse testes.
accelerated cholangiocyte cystogenesis is likely due to overexpression of Cdc25A
Cdc25A activity is required for the metaphase II arrest in mouse oocytes.
deletion of Cdc25a increased apoptosis and accelerated the elimination of DNA damage following UV
In the DNA damage response, instead of inhibiting cyclin B-CDK1 (zeige CDK1 Proteine) through destruction of Cdc25A phosphatase, oocytes utilize an inhibitory phosphorylation of Cdc25B (zeige CDC25B Proteine).
Cdc25A inhibitors block cell-cycle progression and proliferation, reduce liver and kidney weights and cyst growth in animal models of polycystic kidney/liver disease.
CDC25A and CDC25B (zeige CDC25B Proteine) but not CDC25C (zeige CDC25C Proteine) compensate for each other to maintain the proliferative capacity of intestinal epithelial stem and progenitor cells
IL-7 (zeige IL7 Proteine) drives Cdc25A-mediated T-cell proliferation, which prevents the nuclear translocation of Foxo1 (zeige FOXO1 Proteine), leading to reduced expression of CD62L (zeige SELL Proteine) and the migration of T cells into circulation.
Cdc25A is a key player in the developmentally regulated program of apoptosis in X. laevis embryos
Strong ERK (zeige MAPK1 Proteine) activation can target Cdc25A for degradation in a manner similar to, but independent of, Chk1 (zeige CHEK1 Proteine) for cell cycle arrest.
CDC25A is a member of the CDC25 family of phosphatases. CDC25A is required for progression from G1 to the S phase of the cell cycle. It activates the cyclin-dependent kinase CDC2 by removing two phosphate groups. CDC25A is specifically degraded in response to DNA damage, which prevents cells with chromosomal abnormalities from progressing through cell division. CDC25A is an oncogene, although its exact role in oncogenesis has not been demonstrated. Two transcript variants encoding different isoforms have been found for this gene.
cell division cycle 25A
, cell division cycle 25 homolog A
, M-phase inducer phosphatase 1
, Dual specificity phosphatase Cdc25A
, CDC25A2-CAG isoform
, dual specificity phosphatase CDC25A
, dual specificity phosphatase Cdc25A