Usf2 Deficiency Promotes Autophagy to Alleviate Cerebral Ischemia-Reperfusion Injury Through Suppressing YTHDF1-m6A-Mediated Cdc25A Translation. | Usf2 Deficiency Promotes Autophagy to Alleviate Cerebral Ischemia-Reperfusion Injury Through Suppressing YTHDF1-m6A-Mediated Cdc25A Translation. Liu C, Gao Q, Dong J, Cai H. | 05/6/2024 |
CFTR mutation compromises spermatogenesis by enhancing miR-15b maturation and suppressing its regulatory target CDC25Adagger. | CFTR mutation compromises spermatogenesis by enhancing miR-15b maturation and suppressing its regulatory target CDC25A†. Chen Y, Li X, Liao H, Leung X, He J, Wang X, Li F, Yue H, Xu W. | 09/12/2020 |
Our results identify Cdc25A as a potential target for neuroprotectant strategy for the treatment of delayed ischemic neuronal death. | Cdc25A Is a Critical Mediator of Ischemic Neuronal Death In Vitro and In Vivo. Iyirhiaro GO, Im DS, Boonying W, Callaghan SM, During MJ, Slack RS, Park DS., Free PMC Article | 08/19/2017 |
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. | A Genome-wide CRISPR Screen Identifies CDC25A as a Determinant of Sensitivity to ATR Inhibitors. Ruiz S, Mayor-Ruiz C, Lafarga V, Murga M, Vega-Sendino M, Ortega S, Fernandez-Capetillo O., Free PMC Article | 08/5/2017 |
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. | IGF1 regulation of BOULE and CDC25A transcripts via a testosterone-independent pathway in spermatogenesis of adult mice. Gonzalez CR, Dorfman VB, Vitullo AD. | 12/5/2015 |
accelerated cholangiocyte cystogenesis is likely due to overexpression of Cdc25A | Centrosomal abnormalities characterize human and rodent cystic cholangiocytes and are associated with Cdc25A overexpression. Masyuk TV, Lee SO, Radtke BN, Stroope AJ, Huang B, Banales JM, Masyuk AI, Splinter PL, Gradilone SA, Gajdos GB, LaRusso NF., Free PMC Article | 08/23/2014 |
Cdc25A activity is required for the metaphase II arrest in mouse oocytes. | Cdc25A activity is required for the metaphase II arrest in mouse oocytes. Oh JS, Susor A, Schindler K, Schultz RM, Conti M., Free PMC Article | 11/2/2013 |
deletion of Cdc25a increased apoptosis and accelerated the elimination of DNA damage following UV | Accelerated elimination of ultraviolet-induced DNA damage through apoptosis in CDC25A-deficient skin. Yanagida J, Hammiller B, Al-Matouq J, Behrens M, Trempus CS, Repertinger SK, Hansen LA., Free PMC Article | 11/3/2012 |
In the DNA damage response, instead of inhibiting cyclin B-CDK1 through destruction of Cdc25A phosphatase, oocytes utilize an inhibitory phosphorylation of Cdc25B. | Oocytes progress beyond prophase in the presence of DNA damage. Marangos P, Carroll J. | 10/20/2012 |
Cdc25A inhibitors block cell-cycle progression and proliferation, reduce liver and kidney weights and cyst growth in animal models of polycystic kidney/liver disease. | Inhibition of Cdc25A suppresses hepato-renal cystogenesis in rodent models of polycystic kidney and liver disease. Masyuk TV, Radtke BN, Stroope AJ, Banales JM, Masyuk AI, Gradilone SA, Gajdos GB, Chandok N, Bakeberg JL, Ward CJ, Ritman EL, Kiyokawa H, LaRusso NF., Free PMC Article | 05/12/2012 |
CDC25A and CDC25B but not CDC25C compensate for each other to maintain the proliferative capacity of intestinal epithelial stem and progenitor cells | Contributions made by CDC25 phosphatases to proliferation of intestinal epithelial stem and progenitor cells. Lee G, Origanti S, White LS, Sun J, Stappenbeck TS, Piwnica-Worms H., Free PMC Article | 08/6/2011 |
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. | Cdc25A-driven proliferation regulates CD62L levels and lymphocyte movement in response to interleukin-7. Kittipatarin C, Li W, Durum SK, Khaled AR., Free PMC Article | 01/15/2011 |
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. | MiR-322/424 and -503 are induced during muscle differentiation and promote cell cycle quiescence and differentiation by down-regulation of Cdc25A. Sarkar S, Dey BK, Dutta A., Free PMC Article | 01/1/2011 |
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. | DNA damage-induced degradation of Cdc25A does not lead to inhibition of Cdk2 activity in mouse embryonic stem cells. Koledova Z, Kafkova LR, Krämer A, Divoky V. | 06/28/2010 |
The expression of the dual specificity phosphatase CDC25A, is deregulated in Ba/F3 cells expressing the oncogenic protein NPM/ALK and in human cell lines derived from NPM/ALK-positive anaplastic large cell lymphomas. | Upregulation of the CDC25A phosphatase down-stream of the NPM/ALK oncogene participates to anaplastic large cell lymphoma enhanced proliferation. Fernandez-Vidal A, Mazars A, Gautier EF, Prévost G, Payrastre B, Manenti S. | 01/21/2010 |
CDC25A is the only family member to provide an essential function during early embryonic development, and other family members compensate for its loss in adult mice. | Response of small intestinal epithelial cells to acute disruption of cell division through CDC25 deletion. Lee G, White LS, Hurov KE, Stappenbeck TS, Piwnica-Worms H., Free PMC Article | 01/21/2010 |
Results indicate that Cdc25A S123 phosphorylation is crucial for coupling centrosome duplication to DNA replication cycles after DNA damage and therefore is likely to play a role in the regulation of tumorigenesis. | Cdc25A serine 123 phosphorylation couples centrosome duplication with DNA replication and regulates tumorigenesis. Shreeram S, Hee WK, Bulavin DV., Free PMC Article | 01/21/2010 |
Cdc25A promotes G2/M transition in mouse oocytes. | Cdc25A promotes G2/M transition in oocytes. Li M, Yin S, Yuan J, Wei L, Ai JS, Hou Y, Chen DY, Sun QY. | 01/21/2010 |
These data demonstrate that CDC25A behaves differently during female meiosis than during mitosis, and moreover, that CDC25A has a function in resumption of meiosis, spindle formation and the Meiosis I-Meiosis II transition. | CDC25A phosphatase controls meiosis I progression in mouse oocytes. Solc P, Saskova A, Baran V, Kubelka M, Schultz RM, Motlik J., Free PMC Article | 01/21/2010 |
CDC25A is not only a major regulator of both G(1)/S and G(2)/M transition during unperturbed cell cycle progression, but also a critical checkpoint mediator.[review] | CDC25A levels determine the balance of proliferation and checkpoint response. Ray D, Kiyokawa H. | 01/21/2010 |
restricting CDC25A can limit tumorigenesis induced by the HER2/neu-RAS oncogenic pathway without compromising normal cell division or viability [review] | CDC25A phosphatase: a rate-limiting oncogene that determines genomic stability. Ray D, Kiyokawa H. | 01/21/2010 |
TGF-beta stimulates p160ROCK translocation to the nucleus and inhibitory phosphorylation of the cyclin-dependent kinase-activating phosphatase, Cdc25A. | TGF-beta-induced RhoA and p160ROCK activation is involved in the inhibition of Cdc25A with resultant cell-cycle arrest. Bhowmick NA, Ghiassi M, Aakre M, Brown K, Singh V, Moses HL., Free PMC Article | 01/21/2010 |
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. | Cytokine-driven cell cycling is mediated through Cdc25A. Khaled AR, Bulavin DV, Kittipatarin C, Li WQ, Alvarez M, Kim K, Young HA, Fornace AJ, Durum SK., Free PMC Article | 01/21/2010 |
Cdc25A plays a rate-limiting role in transformation and tumor initiation mediated by ras activation | Hemizygous disruption of Cdc25A inhibits cellular transformation and mammary tumorigenesis in mice. Ray D, Terao Y, Nimbalkar D, Hirai H, Osmundson EC, Zou X, Franks R, Christov K, Kiyokawa H. | 01/21/2010 |
A naturally occurring point substitution in Cdc25A, and not Fv2/Stk, is associated with altered cell-cycle status of early erythroid progenitor cells. | A naturally occurring point substitution in Cdc25A, and not Fv2/Stk, is associated with altered cell-cycle status of early erythroid progenitor cells. Melkun E, Pilione M, Paulson RF. | 01/21/2010 |