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Stat3 regulates cell proliferation and axis extension in part via upregulation of Cdc25a expression during oogenesis. Accordingly, restoring Cdc25a expression in stat3 mutants partially suppressed cell proliferation and gastrulation defects.
we uncovered the role of CDC25A in BRCA-mediated tumorigenesis, which can have implications in cancer treatment
Cdc25A negatively regulates the antiviral immune response by inhibiting TBK1 activity.
Study reveals that Cdc25A is elevated, activated and has an essential role in neuronal cell death evoked by apoptotic stimuli relevant to normal development and to AD.
EGFR activation results in c-Src-mediated Cdc25A phosphorylation at Y59, which interacts with nuclear pyruvate kinase M2 (PKM2).
our data also suggests the importance ofLIMD1 and CDC25A in conjunction with HPV for use as diagnostic and prognostic markers of HNSCC, whereas RBSP3 as a prognostic marker only.
Inhibition of YBX1 suppressed lung cancer growth partly via the CDC25a pathway and high expression of YBX1/CDC25a predicts poor prognosis in human lung adenocarcinoma.
MCPH1 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-deficient neuroprogenitors in vivo MCPH1 itself is degraded by APC/CCdh1, but not APC/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-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.
Identify CDC25A as an early cell cycle transducer of FLT3-ITD oncogenic signaling, and as a promising target to inhibit proliferation and re-induce differentiation of FLT3-ITD acute myeloid leukemia cells.
STK38-mediated phosphorylation of CDC25A at Ser-76 and the subsequent degradation of CDC25A are required to promote DNA damage-induced G2/M checkpoint activation.
let-7c suppresses HCC progression, possibly by directly targeting the cell cycle regulator CDC25A and indirectly affecting its downstream target molecules. Let-7c may therefore be an effective therapeutic target for HCC.
Results suggest that miR-449a may act as a tumor suppressor by targeting CDC25A in endometrial cancer.
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 through destruction of Cdc25A phosphatase, oocytes utilize an inhibitory phosphorylation of Cdc25B.
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 but not CDC25C compensate for each other to maintain the proliferative capacity of intestinal epithelial stem and progenitor cells
IL-7 drives Cdc25A-mediated T-cell proliferation, which prevents the nuclear translocation of Foxo1, leading to reduced expression of CD62L and the migration of T cells into circulation.
Results reveal an unexpected role of Cdc25A down-regulation and the inhibitory phosphorylation of cdk2 T14 and Y15 in cell cycle quiescence during muscle differentiation and implicate miRNAs-322 and -503 in the process.
Cdc25A degradation does not inhibit Cdk2 activity because a considerable proportion of Cdk2 molecules localize to the cytoplasm and centrosomes in mESCs, where they may be sheltered from regulation by nuclear Cdc25A.
human papillomavirus type 16 E7 maintains elevated levels of the cdc25A tyrosine phosphatase during deregulation of cell cycle arrest
Identification of epidermal growth factor receptor as a target of Cdc25A protein phosphatase
Studies of a transgenic mouse mammary tumor model identify Cdc25A as a candidate for human tumor latency modifier Apmt2.
A naturally occurring point substitution in Cdc25A, and not Fv2/Stk, is associated with altered cell-cycle status of early erythroid progenitor cells.
TGF-beta stimulates p160ROCK translocation to the nucleus and inhibitory phosphorylation of the cyclin-dependent kinase-activating phosphatase, Cdc25A.
In lymphocyte cell lines dependent on interleukin-3 or interleukin-7, or primary lymphocytes dependent on interleukin 7, the phosphatase Cdc25A is the critical mediator of proliferation.
Chk1/Cdc25A activity participates in activation of a cell cycle pathway-mediated death signal in neurons.
Cdc25A plays a rate-limiting role in transformation and tumor initiation mediated by ras activation
Cdc25A is a key player in the developmentally regulated program of apoptosis in X. laevis embryos
Strong ERK activation can target Cdc25A for degradation in a manner similar to, but independent of, Chk1 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