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CDC25C — PCNA

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: PCNA — CDC25C (direct interaction, two hybrid) Kawabe et al., Oncogene 2002*
• IRef Biogrid Interaction: PCNA — CDC25C (direct interaction, pull down) Kawabe et al., Oncogene 2002*
• IRef Biogrid Interaction: PCNA — CDC25C (physical association, affinity chromatography technology) Kawabe et al., Oncogene 2002*
• IRef Biogrid Interaction: PCNA — CDC25C (physical association, affinity chromatography technology) Ando et al., J Biol Chem 2001*
• IRef Hprd Interaction: PCNA — CDC25C (two hybrid) Kawabe et al., Oncogene 2002*
• IRef Hprd Interaction: PCNA — CDC25C (in vivo) Kawabe et al., Oncogene 2002*
• IRef Hprd Interaction: PCNA — CDC25C (in vitro) Kawabe et al., Oncogene 2002*
• IRef Ophid Interaction: PCNA — CDC25C (aggregation, confirmational text mining) Kawabe et al., Oncogene 2002*
• IRef Ophid Interaction: PCNA — CDC25C (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Blomberg et al., Mol Cell Biol 1999 : In vitro, Cdc25A dephosphorylates and activates the cyclin-Cdk complexes that are active during G ( 1 )
Sandhu et al., Oncogene 2000 : In contrast, in the breast cancer derived MCF-7 line, Cdc25A overexpression increased both cyclin E-cdk2 activity and the S phase fraction
Qian et al., Mol Biol Cell 2001 : In extracts containing fully activated Plx1 and Cdc25C, inhibition of cyclin B-Cdc2 by p21(Cip1) had no significant effect on either the phosphorylation of Cdc25C or the activity of Plx1
Qin et al., Anticancer Res 2004 (Precursor Cell Lymphoblastic Leukemia-Lymphoma) : We speculate that caffeine may enhance MOLT-4 cell entrance into the S-phase through activation of Cdc25 , which in turn activates cyclin dependent protein kinases (CDKs) including CDK2 and drives the cell cycle progression ; while degradation of cyclin E by the ubiquitin/proteasome pathway may account for the decreased levels of cyclin E in these cells
Gu et al., Mol Cancer Ther 2006 (Skin Neoplasms) : Silibinin caused decrease in E2F2 and E2F3 was accompanied by reduced levels of cyclin dependent kinases, cyclins, CDC25C , and mitogen activated protein kinases and Akt signaling and inhibition of cell proliferation
Millar et al., Proc Natl Acad Sci U S A 1991 : CDC25 gene products, like p34CDC2, are localized primarily in the nucleus during interphase, suggesting that activation of p34CDC2/cyclin by p52/p55CDC25 occurs within the nucleus
Ou et al., Mol Nutr Food Res 2010 (Urinary Bladder Neoplasms) : GA-treated cells resulted in significant growth inhibition in a dose dependent manner accompanied by a decrease in cyclin dependent kinases ( Cdk1 ), Cyclin B1, and Cdc25C , but significant increases in p-cdc2 ( Tyr-15 ) and Cip1/p21 by western blotting
Boutros et al., Biol Cell 2011 : CDC25 ( cell division cycle 25 ) phosphatases function as activators of CDK ( cyclin dependent kinase ) -cyclin complexes to regulate progression through the CDC
Walter et al., Mol Biol Cell 1997 : Early MAP kinase activation did not interfere significantly with DNA replication, cyclin synthesis, or association of cyclins with Cdc2, but it did prevent hyperphosphorylation of Cdc25 and Wee1 and activation of Cdc2/cyclin complexes