Regulation of cellular protein quality control networks in a multicellular organism

被引：12

作者：

Bar-Lavan, Yael ^{[1
,2
,3
]}

Kosolapov, Libby ^{[1
,2
]}

Frumkin, Anna ^{[1
,2
]}

Ben-Zvi, Anat ^{[1
,2
]}

机构：

[1] Ben Gurion Univ Negev, Dept Life Sci, IL-84105 Beer Sheva, Israel

[2] Ben Gurion Univ Negev, Natl Inst Biotechnol Negev, IL-84105 Beer Sheva, Israel

[3] Dead Sea & Arava Sci Ctr, Cent Arava Branch, Hazeva, Israel

来源：

FEBS JOURNAL | 2012年 / 279卷 / 04期

基金：

美国国家科学基金会;

关键词：

aging; Caenorhabditis elegans; cell-nonautonomous regulation; heat shock response; HSF1; mitochondrial-specific unfolded protein response; protein misfolding; protein misfolding diseases; proteostasis; stress responses; HEAT-SHOCK RESPONSE; CAENORHABDITIS-ELEGANS; DISEASE; STRESS; SYSTEM; CELLS; PROTEOSTASIS; AGGREGATION; HOMEOSTASIS; GROWTH;

D O I：

10.1111/j.1742-4658.2011.08455.x

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：

The long-term health of all metazoan cells is linked to protein quality control, which is achieved by proteostasis, a complex network of molecular interactions that determines the health of the proteome under physiological or stress conditions. Studying the regulation of cellular proteostasis in the context of the whole organism has unraveled multiple layers of cell-nonautonomous regulation, including neuronal regulation, cell-to-cell stress signals and endocrine signaling that affect growth, development and aging. Here, we discuss emerging concepts in cell-nonautonomous regulation of protein quality control networks. The identification of organismal modulators of cellular proteostasis may present novel, yet general targets for misfolding disease intervention.

引用

页码：526 / 531

页数：6

共 41 条

[1] ATTENUATION OF THE HEAT-SHOCK RESPONSE IN HELA-CELLS IS MEDIATED BY THE RELEASE OF BOUND HEAT-SHOCK TRANSCRIPTION FACTOR AND IS MODULATED BY CHANGES IN GROWTH AND IN HEAT-SHOCK TEMPERATURES [J].