XBP1-KLF9 Axis Acts as a Molecular Rheostat to Control the Transition from Adaptive to Cytotoxic Unfolded Protein Response
Abstract
•XBP1s transcriptionally activates KLF9 under conditions of high ER stress•KLF9 transcriptionally activates TMEM38B and ITPR1 to control ER calcium release•KLF9 further increases ER stress via facilitating calcium release from ER•Klf9 deficiency reduces tunicamycin-induced ER stress in mouse liver Transcription factor XBP1s, activated by endoplasmic reticulum (ER) stress in a dose-dependent manner, plays a central role in adaptive unfolded...
Paper Details
Title
XBP1-KLF9 Axis Acts as a Molecular Rheostat to Control the Transition from Adaptive to Cytotoxic Unfolded Protein Response
Published Date
Oct 1, 2018
Journal
Volume
25
Issue
1
Pages
212 - 223.e4
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History