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BCL2 — PRKAB2

Text-mined interactions from Literome

Cai et al., Free Radic Biol Med 2007 : Overexpression of recombinant human Bcl-2 prevented caspase-3 activation, endogenous Bcl-2 processing, and apoptosis, but did not attenuate oxygen radical formation, AMPK activation, or JNK phosphorylation
Liu et al., J Biol Chem 2010 : Concomitantly, AMPK activation increased the expression of both Bcl-2 and Survivin, two potent anti-apoptotic proteins
Yuan et al., CNS Neurosci Ther 2012 (Glioblastoma) : Subsequently, activated AMPK inhibited mTOR signaling and downregulated antiapoptosis protein Bcl-2 , which was contributed to the additive antiproliferation effects of combination treatment
He et al., Diabetes 2013 (Diabetes Mellitus, Experimental...) : We hypothesized that AMPK induced autophagy ameliorates diabetic cardiomyopathy by inhibiting cardiomyocyte apoptosis and examined the effects of AMPK on the interaction between Beclin1 and Bcl-2 , a switch between autophagy and apoptosis, in diabetic mice and high glucose treated H9c2 cardiac myoblast cells ... Exposure of H9c2 cells to high glucose reduced AMPK activity, inhibited Jun NH2-terminal kinase 1 (JNK1)-B-cell lymphoma 2 (Bcl-2) signaling, and promoted Beclin1 binding to Bcl-2 ... Conversely, activation of AMPK by metformin stimulated JNK1-Bcl-2 signaling and disrupted the Beclin1-Bcl-2 complex
Chen et al., Cell Signal 2013 : Further, after plumbagin treatment, activated AMPK directly phosphorylates Raptor to inhibit mTOR complex 1 (mTORC1) activation and Bcl-2 expression in colon cancer cells