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The role of UPR in cell death upon prolonged ER stress. Prolonged activation of UPR can promote apoptosis. Dimerization and phosphorylation of PERK promotes ATF4, which activates CHOP and subsequently apoptosis. ATF6 can also promote upregulation of CHOP. IRE1α can promote apoptosis via activation of JNK and via degradation of pro-survival RNAs by RIDD.
