Quality Control of Mitochondrial Proteostasis

被引：190

作者：

Baker, Michael J. ^{[1
]}

Tatsuta, Takashi ^{[1
]}

Langer, Thomas ^{[1
,2
]}

机构：

[1] Univ Cologne, Inst Genet, Cologne Excellence Cluster Cellular Stress Respon, Ctr Mol Med CMMC, D-50674 Cologne, Germany

[2] Max Planck Inst Biol Aging, D-50931 Cologne, Germany

来源：

COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY | 2011年 / 3卷 / 07期

基金：

欧洲研究理事会;

关键词：

M-AAA PROTEASE; HEREDITARY SPASTIC PARAPLEGIA; YEAST SACCHAROMYCES-CEREVISIAE; ATP-DEPENDENT PROTEASE; CYTOCHROME-C RELEASE; ABC-TRANSPORTER MDL1; HEAT-SHOCK-PROTEIN; LON PROTEASE; NEURODEGENERATIVE DISEASES; MEMBRANE-PROTEINS;

D O I：

10.1101/cshperspect.a007559

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

A decline in mitochondrial activity has been associated with aging and is a hallmark of many neurological diseases. Surveillance mechanisms acting at the molecular, organellar, and cellular level monitor mitochondrial integrity and ensure the maintenance of mitochondrial proteostasis. Here we will review the central role of mitochondrial chaperones and proteases, the cytosolic ubiquitin-proteasome system, and the mitochondrial unfolded response in this interconnected quality control network, highlighting the dual function of some proteases in protein quality control within the organelle and for the regulation of mitochondrial fusion and mitophagy.

引用

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页码：1 / 19

页数：19

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