期刊
MOLECULAR & CELLULAR ONCOLOGY
卷 6, 期 6, 页码 -出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/23723556.2019.1659078
关键词
Word; ER stress; UPR; IRE1 alpha; MITOL; MARCH5; ER-mitochondria contact site
类别
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 1 alpha (IRE1 alpha), 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.
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