Unfolded protein response (UPRs) directs adaption or apoptosis depending on the severity of endoplasmic-reticulum (ER) stress. We found that apoptotic signaling by inositol requiring enzyme 1α (IRE1α), a transducer of UPRs, is suppressed by mitochondrial ubiquitin ligase MITOL/MARCH5 on ER-mitochondria contacts, suggesting that mitochondria regulate cell fate under ER stress.
Keywords: ER stress; ER-mitochondria contact site; IRE1α; MITOL/MARCH5; UPR; Word.
© 2019 The Author(s). Published with license by Taylor & Francis Group, LLC.