Transient overexpression of Werner protein rescues starvation induced autophagy in Werner syndrome cells

被引：13

作者：

Maity, Jyotirindra ^{[1
]}

Bohr, Vilhelm A. ^{[2
]}

Laskar, Aparna ^{[3
]}

Karmakar, Parimal ^{[1
]}

机构：

[1] Jadavpur Univ, Dept Life Sci & Biotechnol, Kolkata 700032, India

[2] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA

[3] CSIR, Indian Inst Chem Biol, Kolkata 700032, India

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2014年 / 1842卷 / 12期

关键词：

Autophagy; Aging; Beclin-1; RecQ helicase; Werner protein; Werner syndrome; RNA-POLYMERASE-I; RECQ HELICASES; MAMMALIAN TARGET; DNA-DAMAGE; WRN; EXPRESSION; MTOR; PHOSPHORYLATION; RECOMBINATION; TUMORIGENESIS;

D O I：

10.1016/j.bbadis.2014.09.007

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：

Reduced autophagy may be associated with normal and pathological aging. Here we report a link between autophagy and Werner protein (WRNp), mutated in Werner syndrome, the human premature aging Werner syndrome (WS). WRN mutant fibroblast AG11395 and AG05229 respond weakly to starvation induced autophagy compared to normal cells. While the fusion of phagosomes with lysosome is normal, WS cells contain fewer autophagy vacuoles. Cellular starvation autophagy in WS cells is restored after transfection with full length WRN. Further, siRNA mediated silencing of WRN in the normal fibroblast cell line WI-38 results in decreased autophagy and altered expression of autophagy related proteins. Thus, our observations suggest that WRN may have a role in controlling autophagy and hereby cellular maintenance. (C) 2014 Elsevier B.V. All rights reserved.

引用

页码：2387 / 2394

页数：8

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