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BCL2 — GRAP2

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Lakics et al., J Immunol 2000 : More strikingly, LPS induced phosphorylation of p38 mitogen activated protein kinase and c-Jun N-terminal kinase was strongly repressed by Bcl-xL overexpression, offering a possible mechanism for the inhibition of LPS induced cytokine production
Kaiser et al., J Biol Chem 2004 (Reperfusion Injury) : In primary neonatal cardiomyocyte cultures, adenoviral mediated gene transfer of a p38 inhibitory mutant up-regulated Bcl-2, whereas expression of an activated p38 mutant down-regulated Bcl-2 protein levels
Wang et al., Chin J Physiol 2007 : Scutellarin decreased caspase-3 activity, increased Bcl-XL expression, inhibited p38 phosphorylation and attenuated ROS production
Chen et al., Toxicology 2009 (Neuroblastoma) : SB202190 ( p38 MAPK inhibitor ) and SP600125 ( JNK inhibitor ) attenuated mitochondrial depolarization, degradation of Bcl-2/Bcl-xL , and mitochondrial translocation of Bax
Harnett et al., Cell Biochem Funct 2013 : Interestingly, Bcl-xL expression inhibited p38 activation, but Z-VAD-fmk treatment did not, indicating that activation of this MAPK occurs downstream of mitochondrial dysfunction and is independent of caspases