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FHL1 increase inhibitory CDC25 phosphorylation by forming a complex with CHK2 and CDC25, and sequester CDC25 in the cytoplasm by forming another complex with 14-3-3 and CDC25, resulting in increased radioresistance in cancer cells.
CDC25A plays a novel role in regulating the malignant behavior of glioma stem cells as a part of Linc00152/miR-103a-3p/FEZF1/CDC25A axis.
Overexpression of the CDK1 and CDC25A may have a role in the pathogenesis of the NFPA.
Mdm2 overexpression and Cdc25C downregulation delay cell cycle progression through the G2/M phase.
Xanthatin functions as a DNA-damaging agent in non-small cell lung carcinomas by activating Chk1-mediated DDR and lysosome-mediated degradation of Cdc25C.
Myelodysplastic syndrome -related P95 point mutants of SRSF2 lead to alternative splicing of CDC25C in a manner that is not dependent on the DNA damage response.
The aim of this review is to shed light on the role of four different phosphatases (PTEN, PP2A, CDC25 and DUSP1) in five different solid tumors (breast cancer, lung cancer, pancreatic cancer, prostate cancer and ovarian cancer), in order to better understand the most frequent and aggressive primary cancer of the central nervous system, glioblastoma.
Data show that TRIB2-mediated degradation of CDC25C is associated with lysine-48-linked CDC25C polyubiquitination driven by the TRIB2 kinase-like domain.
High expression of pCHK2-Thr68 was associated with decreased patient survival (p = 0.001), but was not an independent prognostic factor. Our results suggest that pCHK2-Thr68 and pCDC25C-Ser216 play important roles in breast cancer and may be potential treatment targets
the biology of the activation/deactivation of CDC25 by kinases/phosphatases to maintain the level of CDK-cyclin activities and thus the genomic stability
the knockdown of CDC25C can reduce both the radiotherapy sensitivity and the proliferation activity of EC9706 cells.
results identify CDC25C as a downstream target of the mutated tyrosine kinase FLT3-ITD affecting cell-cycle regulation in a model of AML
Suggest that the p53-p21-DREAM-CDE/CHR pathway regulates p53-dependent repression of Survivin, CDC25C, and PLK1 in HCT116 cells.
Data indicate that nine compounds were identified with Ki values for CDC25A, -B and -C ranging from 0.01 to 4.4 muM.
These miR-142-3p functioned as a tumor suppressor by targeting CDC25C.
Cdc25C negatively regulates proapoptotic ASK1 in a cell cycle-dependent manner and may play a role in G2/M checkpoint-mediated apoptosis.
Recurrent CDC25C mutations drive malignant transformation in familial platelet disorder to acute myelogenous leukaemia.
CDC25C seems important for the phenotype of AML cells at least for a subset of patients. Many of the identified CDC25 inhibitors show cross-reactivity among the three CDC25 isoforms.
for the first time, we demonstrated that CTD induced G2/M phase arrest via the inhibition of Cdc25c and cyclin A and induced apoptosis was through death receptor (extrinsic), intrinsic (mitochondria) and ER stress pathways in A375. S2 cells.
we conclude that inhibition of KIF22 suppresses cancer cell proliferation by delaying mitotic exit through the transcriptional upregulation of CDC25C.
oxidative stress-induced DNA damage of mouse zygotes triggers the cell cycle checkpoint, which results in G2/M cell cycle arrest, and that phospho-Cdc25B (Ser323), phospho-Cdc25C (Ser216), and phospho-Cdc2 (Tyr15) participate in activating the G2/M checkpoint.
The role of Cdc25c and Cdc25b in activating G2/M cell cycle checkpoint in zygote.
an asymmetrical distribution pattern for Cdc25c transcripts in 2-cell embryos.
CDC25A and CDC25B but not CDC25C compensate for each other to maintain the proliferative capacity of intestinal epithelial stem and progenitor cells
A single cell cycle genes homology region controls transcription of the cdc25C gene and is able to cooperate with E2F or Sp1/3 sites
Cdc25A, or possibly other phosphatases, is able to functionally compensate for the loss of Cdc25B and Cdc25C in mice
The present study was aimed to investigate the possibility that selenium (Se)-induced oxidative stress mediated alterations in Cdc25c and p21 may cause modulations in the CDC2/Cyclin B1 complex responsible for G2/M phase checkpoint in spermatogenesis.
In Lzts1(-/-) mouse embryo fibroblasts (MEFs), Cdc25C degradation was increased during M phase, resulting in decreased Cdk1 activity.
PP2A:B56delta as a key upstream regulator of Cdk1 activity upon exit from mitosis
Blocking mitotic entry by adding the catalytic subunit of protein kinase A results in increased wee1 Ser549 phosphorylation and maintenance of cdc25C.
These observations identify PP2A/B56delta as a central checkpoint effector and suggest a mechanism for controlling 14-3-3 interactions to promote mitosis.
In Xenopus oocytes, p42 MAPK interacts with hypophosphorylated Cdc25 before meiotic induction. During meiotic induction, p42 MAPK phosphorylates Cdc25 at three sites, increasing Cdc25's phosphatase activity.
This gene is highly conserved during evolution and it plays a key role in the regulation of cell division. The encoded protein is a tyrosine phosphatase and belongs to the Cdc25 phosphatase family. It directs dephosphorylation of cyclin B-bound CDC2 and triggers entry into mitosis. It is also thought to suppress p53-induced growth arrest. Multiple alternatively spliced transcript variants of this gene have been described, however, the full-length nature of many of them is not known.
cell division cycle 25 homolog C (S. pombe)
, m-phase inducer phosphatase 3-like
, cell division cycle 25 homolog C
, cell division cycle 25C
, Dual specificity phosphatase Cdc25C
, M-phase inducer phosphatase 3
, dual specificity phosphatase Cdc25C
, dual specificity phosphatase CDC25C
, mitosis inducer CDC25
, phosphotyrosine phosphatase
, protein phosphatase 1, regulatory subunit 60
, cell cycle phosphatase CDC25C
, cell division cycle control protein 25C