One of the important signaling mediators in the ER stress-mediated apoptosis pathway is CHOP [ 15, 29].
Because oxLDL trigger a prolonged ER stress activation, which may have a role in apoptotic cell death through IRE1 α-TRAF2-JNK pathway and CHOP expression, we checked the activation of these proapoptotic pathways in hVSMC.
In the context of our studies, statin exposure could trigger UPR and Bcl-2 protein-mediated apoptosis via pathways involving CHOP.
Moreover, further prospective studies are needed to determine the specific RBPs and their binding sites in FGF21 3′-UTR as well as the signaling pathway of CHOP- dependent activation of FGF21 in ER stress.
Being a pro-apoptosis factor, Bim is activated via the JNK and p38 kinase pathways and CHOP during endoplasmic reticulum (ER) stress, which can be stimulated by viral infection, and has been reported to directly link ER stress to mitochondrial apoptosis in cells expressing mSOD1.
These results suggest that followed CHOP pathway, the caspase apoptosis pathway was activated after ER stress due to Ctm-PrP accumulation.
It has been shown that trib3 is induced via the ATF4-CHOP pathway through the identification of a CHOP-binding site in the proximal portion of the promoter [ 53].
Recently, a new pathway linking the Chop branch of the UPR to apoptosis was described where Chop, through endoplasmic reticulum oxidoreductin 1 alpha induction, activates inositol trisphosphate receptor-mediated ER calcium release and triggers apoptosis.
However, whether EEP protects macrophages from ox-LDL-induced apoptosis by inhibiting endoplasmic reticulum (ER) stress-C/EBP homologous protein (CHOP) pathway has not yet been determined.
These data suggest that there are context-dependent disparate stress responses to the drug combination, and the JNK pathway, but not CHOP, can be critically involved in the synergistic combination effect in certain cancer cell types.
Of importance, we show that mRNA levels of ER stress markers of the PERK CHOP pathway, ATF4 and CHOP, are significantly increased in c9ALS cases compared to sporadic ALS cases without the C9ORF72 repeat expansion.
