BiP binding keeps ATF6 at bay
- PMID: 12110159
- DOI: 10.1016/s1534-5807(02)00210-1
BiP binding keeps ATF6 at bay
Abstract
A study by, in this issue of Developmental Cell shows that transport to the Golgi complex and subsequent proteolytic activation of the stress-regulated transcription factor ATF6 is initiated by the dissociation of the ER chaperone BiP from ATF6. This demonstrates that BiP is a key element in sensing the folding capacity within the ER and provides mechanistic insights on how the activation of membrane-bound transcription factors can be regulated.
Comment on
-
ER stress regulation of ATF6 localization by dissociation of BiP/GRP78 binding and unmasking of Golgi localization signals.Dev Cell. 2002 Jul;3(1):99-111. doi: 10.1016/s1534-5807(02)00203-4. Dev Cell. 2002. PMID: 12110171
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
