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BCL2 — POLDIP2

Text-mined interactions from Literome

de la Monte et al., J Alzheimers Dis 2000 : H2O2-treatment resulted in dose dependent increases in cell death due to genomic and mitochondrial DNA damage associated with increased levels of 8-OHdG and the p53 and CD95 pro-apoptosis genes, reduced levels of the Bcl-2 survival gene, activation of JNK and p38 stress kinases, and inhibition of PI3 kinase survival signaling
Kaiser et al., J Biol Chem 2004 (Reperfusion Injury) : Mechanistically, inhibition of p38 signaling promoted a dramatic up-regulation of Bcl-2 in the hearts of transgenic mice
Ki et al., Am J Physiol Gastrointest Liver Physiol 2008 : Despite its cytoprotective effect, SB-203580, a p38 inhibitor, was unlikely to reduce VacA induced Bax dimerization and rather inhibited villin and Bcl2 expression, indicating that p38 may also play a role in cell proliferation or differentiation for survival after VacA intoxication
Nencioni et al., J Biol Chem 2009 : In infected Bcl-2 ( + ) cells, activated p38MAPK was found predominantly in the cytoplasm, colocalized with Bcl-2, and both Bcl-2 phosphorylation and virally induced apoptosis were diminished by specific inhibition of p38MAPK activity
Peart et al., Rejuvenation Res 2012 (Ischemia...) : CR counters age effects on postischemic dysfunction/cell death ; this is associated with reversal of age effects on p70S6K, augmentation of Akt and Bcl2 levels, and preischemic p38-MAPK activation