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BCL2 — FOS

Text-mined interactions from Literome

Feng et al., Oncogene 2004 (MAP Kinase Signaling System) : Inhibition of the activities of these kinases or the upstream activating kinases by pharmacological inhibitors or dominant negative mutants abolishes the Bcl-2 mediated regulation of AP-1 , LEDGF and their downstream genes
Marrero et al., Brain Res 2009 (Inflammation) : In this study, we investigated the effects of inhibiting the alpha7 nAChR-JAK2 pro-survival cascade on the nicotine induced production of the survival factor Bcl-2 and the transcriptional activation of NF-kappaB, AP-1 , STAT1, STAT3, and STAT5
Gillardon et al., Brain Res Mol Brain Res 1996 (Arterial Occlusive Diseases...) : These findings suggest that a shift in the ratio of cell death repressor Bcl-2 to cell death effector Bax and a concomitant activation of c-Fos may contribute to neuronal apoptosis in the infarcted thalamus and cortex
He et al., J Biol Chem 1998 : Also, overexpression of Bcl-2 in WEHI7.2 cells blocked c-Fos degradation and inhibited apoptosis