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Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis
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Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis
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Journal Article
Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis
2018
Overview
Cellular homoeostatic pathways such as macroautophagy (hereinafter autophagy) are regulated by basic mechanisms that are conserved throughout the eukaryotic kingdom. However, it remains poorly understood how these mechanisms further evolved in higher organisms. Here we describe a modification in the autophagy pathway in vertebrates, which promotes its activity in response to oxidative stress. We have identified two oxidation-sensitive cysteine residues in a prototypic autophagy receptor SQSTM1/p62, which allow activation of pro-survival autophagy in stress conditions. The
Drosophila
p62 homologue, Ref(2)P, lacks these oxidation-sensitive cysteine residues and their introduction into the protein increases protein turnover and stress resistance of flies, whereas perturbation of p62 oxidation in humans may result in age-related pathology. We propose that the redox-sensitivity of p62 may have evolved in vertebrates as a mechanism that allows activation of autophagy in response to oxidative stress to maintain cellular homoeostasis and increase cell survival.
The cellular mechanisms underlying autophagy are conserved; however it is unclear how they evolved in higher organisms. Here the authors identify two oxidation-sensitive cysteine residues in the autophagy receptor SQSTM1/p62 in vertebrates which allow activation of pro-survival autophagy in stress conditions.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/106
/ 13/109
/ 13/51
/ 14/19
/ 14/35
/ 64
/ 64/24
/ Age
/ Animals
/ Cell Survival - drug effects
/ Cysteine
/ Drosophila melanogaster - cytology
/ Drosophila melanogaster - genetics
/ Drosophila melanogaster - metabolism
/ Homology
/ Humanities and Social Sciences
/ Humans
/ Hydrogen Peroxide - pharmacology
/ Oxidants
/ Proteins
/ Reactive Oxygen Species - metabolism
/ Residues
/ Science
/ Sequence Homology, Amino Acid
/ Sequestosome-1 Protein - genetics
/ Sequestosome-1 Protein - metabolism
/ Survival
