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BCL2 — DDIT3
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Tiwary et al., PloS one 2010
:
Knockdown studies using siRNAs to TRAIL, DR5, JNK and CHOP as well as chemical inhibitors of ER stress and caspase-8 showed that : i ) alpha-TEA activation of DR5/caspase-8 induces an ER stress mediated JNK/CHOP/DR5 positive amplification loop ; ii ) alpha-TEA downregulation of c-FLIP ( L ) protein levels is mediated by JNK/CHOP/DR5 loop via a JNK dependent Itch E3 ligase ubiquitination that further serves to enhance the JNK/CHOP/DR5 amplification loop by preventing c-FLIP 's inhibition of caspase-8 ; and ( iii ) alpha-TEA downregulation of
Bcl-2 is
mediated by the ER stress dependent
JNK/CHOP/DR5 signaling ... Taken together, ER stress plays an important role in alpha-TEA induced apoptosis by enhancing DR5/caspase-8 pro-apoptotic signaling and suppressing anti-apoptotic factors c-FLIP and
Bcl-2 via ER stress
mediated JNK/CHOP/DR5/caspase-8 signaling
Pan et al., Toxicol Appl Pharmacol 2012
(Breast Neoplasms) :
In addition, prodigiosin down-regulated
BCL2 in a
CHOP dependent manner ... Importantly, restoration of BCL2 expression blocked prodigiosin induced PARP cleavage and greatly enhanced the survival of prodigiosin treated cells, suggesting that
CHOP dependent
BCL2 suppression mediates prodigiosin elicited cell death ... Mechanistically, prodigiosin engages the IRE1-JNK and PERK-eIF2a branches of the UPR signaling to up-regulate
CHOP , which in turn
mediates BCL2 suppression to induce cell death