Endoplasmic reticulum stress activates telomerase.
Author: Zhou J, Mao B, Zhou Q, Ding D, Wang M, Guo P, Gao Y, Shay JW, Yuan Z, Cong YS.
Affiliation:
Institute of Aging Research, Hangzhou Normal University School of Medicine, Hangzhou, 310036, China; Key Laboratory for Cell Proliferation and Regulation Biology of Ministry of Education, Beijing Normal University, Beijing, 100875, China.
Conference/Journal: Aging Cell.
Date published: 2013 Oct 9
Other:
Special Notes: doi: 10.1111/acel.12161 , Word Count: 125
Telomerase contributes to cell proliferation and survival through both telomere-dependent and telomere-independent mechanisms. In this report, we discovered that ER (endoplasmic reticulum) stress transiently activates the catalytic components of telomerase (TERT) expression in human cancer cell lines and murine primary neural cells. Importantly, we show that depletion of hTERT sensitizes cells to undergo apoptosis under ER stress, whereas increased hTERT expression reduces ER stress-induced cell death independent of catalytically active enzyme or DNA damage signaling. Our findings establish a functional link between ER stress and telomerase, both of which have important implications in the pathologies associated with aging and cancer. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
hTERT , ER stress, Telomerase, apoptosis
PMID: 24119029
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