Loss of ATF6α in a human carcinoma cell line is compensated not by its paralogue ATF6β but by sustained activation of the IRE1 and PERK arms for tumor growth in nude mice-Reference-Cited by-同舟云学术

Loss of ATF6α in a human carcinoma cell line is compensated not by its paralogue ATF6β but by sustained activation of the IRE1 and PERK arms for tumor growth in nude mice

Published:2023-03-01 Issue:3 Volume:34 Page:
ISSN:1059-1524
Container-title:Molecular Biology of the Cell
language:en
Short-container-title:MBoC

Author:

Jin Shengyu¹,Jin Byungseok¹,Ishikawa Tokiro¹,Ninagawa Satoshi¹,Okada Tetsuya¹,Koyasu Sho¹,Harada Hiroshi²,Mori Kazutoshi¹

Affiliation:

1. Department of Biophysics, Graduate School of Science, Kyoto University, Kyoto 606-8502, Japan

2. Laboratory of Cancer Cell Biology, Graduate School of Biostudies, Kyoto University, Kyoto 606-8501, Japan

Abstract

Tumor cells activate the unfolded protein response for growth. We investigated the requirement for the ATF6 arm, consisting of ubiquitously expressed ATF6α and ATF6β, and found that the loss of ATF6α in tumor cells resulted in sustained activation of the IRE1 and PERK arms, contrary to the expectation from our analysis of mouse embryonic fibroblasts.

Publisher

American Society for Cell Biology (ASCB)

Subject

Cell Biology,Molecular Biology

Reference48 articles.

1. ATF6 Is a Transcription Factor Specializing in the Regulation of Quality Control Proteins in the Endoplasmic Reticulum

2. Hypoxia, endoplasmic reticulum stress and chemoresistance: dangerous liaisons

3. ER stress-regulated translation increases tolerance to extreme hypoxia and promotes tumor growth

4. Molecular Chaperones and Protein Quality Control

5. IRE1 couples endoplasmic reticulum load to secretory capacity by processing the XBP-1 mRNA

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