A close connection between the PERK and IRE arms of the UPR and the transcriptional regulation of autophagy

被引：50

作者：

Deegan, Shane ^{[1
,2
]}

Koryga, Izabela ^{[1
,2
]}

Glynn, Sharon A. ^{[1
,3
]}

Gupta, Sanjeev ^{[1
,4
]}

Gorman, Adrienne M. ^{[1
,2
]}

Samali, Afshin ^{[1
,2
]}

机构：

[1] Natl Univ Ireland Galway, Apoptosis Res Ctr, Galway, Ireland

[2] Natl Univ Ireland Galway, Sch Nat Sci, Galway, Ireland

[3] Natl Univ Ireland Galway, Prostate Canc Inst, Galway, Ireland

[4] Natl Univ Ireland Galway, Sch Med, Galway, Ireland

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2015年 / 456卷 / 01期

基金：

爱尔兰科学基金会;

关键词：

Autophagy; ER stress; IRE1; PERK; Unfolded protein response (UPR); ENDOPLASMIC-RETICULUM STRESS; INDUCED APOPTOSIS; DEGRADATION; NIX;

D O I：

10.1016/j.bbrc.2014.11.076

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Endoplasmic reticulum (ER) stress is known to lead to activation of both the unfolded protein response (UPR) and autophagy. Although regulatory connections have been identified between the UPR and autophagy, it is still unclear to what extent the UPR regulates the genes involved at the different stages of the autophagy pathway. Here, we carried out a microarray analysis of HCT116 cells subjected to ER stress and observed the transcriptional upregulation of a large cohort of autophagy-related genes. Of particular interest, we identified the transcriptional upregulation of the autophagy receptor genes SQSTM1/p62, NBR1 and BNIP3L/NIX in response to ER stress and show that the inhibition of the UPR transmembrane receptors, PERK and IRE1, abrogates this upregulation. (C) 2014 Elsevier Inc. All rights reserved.

引用

页码：305 / 311

页数：7

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