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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