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Human CDC25A Protein expressed in Escherichia coli (E. coli) - ABIN667374
Suorensen, Syljuuasen, Falck, Schroeder, Roennstrand, Khanna, Zhou, Bartek, Lukas: Chk1 regulates the S phase checkpoint by coupling the physiological turnover and ionizing radiation-induced accelerated proteolysis of Cdc25A. in Cancer cell 2003
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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 Proteins)-ITD oncogenic signaling, and as a promising target to inhibit proliferation and re-induce differentiation of FLT3 (show FLT3 Proteins)-ITD acute myeloid leukemia (show BCL11A Proteins) 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 Proteins) 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 Proteins).
Results suggest that miR-449a may act as a tumor suppressor by targeting CDC25A in endometrial cancer.
CDC25C (show CDC25C Proteins) seems important for the phenotype of AML (show RUNX1 Proteins) cells at least for a subset of patients. Many of the identified CDC25 (show RASGRF1 Proteins) inhibitors show cross-reactivity among the three CDC25 (show RASGRF1 Proteins) isoforms.
Our results suggest that expression of CDC25B (show CDC25B Proteins) may be used as a potential prognostic marker in the pathogenesis of retinoblastoma.
These results suggest that Cdc25a promotes human cytomegalovirus replication and elevation of Cdc25a levels after human cytomegalovirus infection are due in part to human cytomegalovirus-mediated repression of miR (show MLXIP Proteins)-21.
miR-424(322)/503-dependent posttranscriptional downregulation of CDC25A cooperates with transcriptional repression of the CDC25A promoter and proteasome-mediated degradation to reduce the levels of CDC25A expression and to induce cell cycle arrest.
Findings suggest that inhibition of H19 long non-coding RNA (LncRNAH19) and miR-675 expression can promote migration and invasion of hepatocellular carcinoma (HCC) cells via AKT/GSK-3beta/Cdc25A signaling pathway.
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 (show CDK1 Proteins) through destruction of Cdc25A phosphatase, oocytes utilize an inhibitory phosphorylation of Cdc25B (show CDC25B Proteins).
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 Proteins) but not CDC25C (show CDC25C Proteins) compensate for each other to maintain the proliferative capacity of intestinal epithelial stem and progenitor cells
IL-7 (show IL7 Proteins) drives Cdc25A-mediated T-cell proliferation, which prevents the nuclear translocation of Foxo1 (show FOXO1 Proteins), leading to reduced expression of CD62L (show SELL Proteins) 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 Proteins) T14 (show CD27 Proteins) 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 Proteins) activation can target Cdc25A for degradation in a manner similar to, but independent of, Chk1 (show CHEK1 Proteins) 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