Anti-CDC25C monoclonal antibody (DCABY-1053)

Specifications


Host Species
Mouse
Antibody Isotype
IgG1
Clone
344DU0.7.7
Species Reactivity
Human
Conjugate
Unconjugated

Applications


Application Notes
WB: 1:1000-8000
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
CDC25C; M-phase inducer phosphatase 3; Dual specificity phosphatase Cdc25C
Entrez Gene ID
UniProt ID

Product Background


Pathway
Activation of ATR in response to replication stress; Cell Cycle; Cell Cycle Checkpoints; Cell Cycle, Mitotic; Cell cycle; Chk1/Chk2(Cds1) mediated inactivation of Cyclin B:Cdk1 complex; Cyclin A/B1 associated events during G2/M transition; Cyclin B2 mediated events;

Citations


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References


Genome-wide pathway analysis of a genome-wide association study on Alzheimer's disease

NEUROLOGICAL SCIENCES

Authors: Lee, Young Ho; Song, Gwan Gyu

The aims of this study were to identify candidate single nucleotide polymorphisms (SNPs) and mechanisms of Alzheimer's disease (AD) and to generate SNP to gene to pathway hypotheses. An AD genome-wide association study (GWAS) dataset that included 370,542 SNPs in 1,000 cases and 1,000 controls of European descent was used in this study. Identify Candidate Causal SNPs and Pathway (ICSNPathway) analysis was applied to the GWAS dataset. ICSNPathway analysis identified 3 candidate SNPs and 2 pathways, which provided 3 hypothetical biological mechanisms. The strongest hypothetical biological mechanism was rs8076604 [non-synonymous coding (deleterious)] to MYO18A to negative regulation of programmed cell death [nominal P < 0.001, false discovery rate (FDR) < 0.043]. The second was rs2811226 (regulatory region) to ANXA1 to negative regulation of programmed cell death (nominal P < 0.001, FDR 0.043). The third was rs3734166 (non-synonymous coding) to CDC25C to M phase of the mitotic cell cycle (nominal P < 0.001, FDR 0.049). By applying the ICSNPathway analysis to the AD GWAS meta-analysis data, three candidate SNPs, three genes (MYO18A, ANXA1, CDC25C), 2 pathways involving negative regulation of programmed cell death and 1 pathway involving the M phase of the mitotic cell cycle were identified, which may contribute to AD susceptibility.

BRCA1-dependent Chk1 phosphorylation triggers partial chromatin disassociation of phosphorylated Chk1 and facilitates S-phase cell cycle arrest

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY

Authors: Yarden, Ronit I.; Metsuyanim, Sally; Pickholtz, Itay; Shabbeer, Shabana; Tellio, Hadass; Papa, Moshe Z.

Chk1 phosphorylation by the PI3-like kinases ATR and ATM is critical for its activation and its role in prevention of premature mitotic entry in response to DNA damage or stalled replication. The breast and ovarian tumor suppressor, BRCA1, is among several checkpoint mediators that are required for Chk1 activation by ATM and AIR. Previously we showed that BRCA1 is necessary for Chk1 phosphorylation and activation following ionizing radiation. BRCA1 has been implicated in S-phase checkpoint control yet its mechanism of action is not well characterized. Here we report that BRCA1 is critical for Chk1 phosphorylation in response to inhibition of replication by either cisplatin or hydroxyurea. While Chk1 phosphorylation of S317 is fully dependent on BRCA1, additional proteins may mediate S345 phosphorylation at later time points. In addition, we show that a subset of phosphorylated Chk1 is released from the chromatin in a BRCA1-dependent manner which may lead to the phosphorylation of Chk1 substrate, Cdc25C, on S216 and to S-phase checkpoint activation. Inhibition of Chk1 kinase by UCN-01 or expression of Chk1 phosphorylation mutants in which the serine residues were substituted with alanine residues abrogates BRCA1-dependent cell cycle arrest in response replication inhibition. These data reveal that BRCA1 facilitates Chk1 phosphorylation and its partial chromatin dissociation following replication inhibition that is likely to be required for S-phase checkpoint signaling. (C) 2012 Elsevier Ltd. All rights reserved.

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