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Stat3 (show STAT3 ELISA Kits) regulates cell proliferation and axis extension in part via upregulation of Cdc25a expression during oogenesis. Accordingly, restoring Cdc25a expression in stat3 (show STAT3 ELISA Kits) mutants partially suppressed cell proliferation and gastrulation defects.
The expression level of Cdc25A was significantly increased (<0.05) after treatment with miR (show MLXIP ELISA Kits)-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 (show FLT3 ELISA Kits)-ITD oncogenic signaling, and as a promising target to inhibit proliferation and re-induce differentiation of FLT3 (show FLT3 ELISA Kits)-ITD acute myeloid leukemia (show BCL11A ELISA Kits) 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 (show FAM126A ELISA Kits) 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 (show FAM126A ELISA Kits).
Results suggest that miR-449a may act as a tumor suppressor by targeting CDC25A in endometrial cancer.
CDC25C (show CDC25C ELISA Kits) seems important for the phenotype of AML (show RUNX1 ELISA Kits) cells at least for a subset of patients. Many of the identified CDC25 (show RASGRF1 ELISA Kits) inhibitors show cross-reactivity among the three CDC25 (show RASGRF1 ELISA Kits) isoforms.
These results showed that IGF1 (show IGF1 ELISA Kits) regulated the expression of BOULE (show BOLL ELISA Kits) and CDC25A mRNAs via ERK1/2 (show MAPK1/3 ELISA Kits) 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 (show CDK1 ELISA Kits) through destruction of Cdc25A phosphatase, oocytes utilize an inhibitory phosphorylation of Cdc25B (show CDC25B ELISA Kits).
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 (show CDC25B ELISA Kits) but not CDC25C (show CDC25C ELISA Kits) compensate for each other to maintain the proliferative capacity of intestinal epithelial stem and progenitor cells
IL-7 (show IL7 ELISA Kits) drives Cdc25A-mediated T-cell proliferation, which prevents the nuclear translocation of Foxo1 (show FOXO1 ELISA Kits), leading to reduced expression of CD62L (show SELL ELISA Kits) and the migration of T cells into circulation.
Results reveal an unexpected role of Cdc25A down-regulation and the inhibitory phosphorylation of cdk2 (show CDK2 ELISA Kits) T14 (show CD27 ELISA Kits) 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.
Cdc25A is a key player in the developmentally regulated program of apoptosis in X. laevis embryos
Strong ERK (show MAPK1 ELISA Kits) activation can target Cdc25A for degradation in a manner similar to, but independent of, Chk1 (show CHEK1 ELISA Kits) 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