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Evidence against Stable Protein S-Nitrosylation as a Widespread Mechanism of Post-translational Regulation
S-nitrosation, commonly referred to as S-nitrosylation, is widely regarded as a ubiquitous, stable post-translational modification that directly regulates many proteins. Such a widespread role would appear to be incompatible with the inherent lability of the S-nitroso bond, especially its propensity...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cell Press
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5807093/ https://www.ncbi.nlm.nih.gov/pubmed/29358077 http://dx.doi.org/10.1016/j.molcel.2017.12.019 |
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author | Wolhuter, Kathryn Whitwell, Harry J. Switzer, Christopher H. Burgoyne, Joseph R. Timms, John F. Eaton, Philip |
author_facet | Wolhuter, Kathryn Whitwell, Harry J. Switzer, Christopher H. Burgoyne, Joseph R. Timms, John F. Eaton, Philip |
author_sort | Wolhuter, Kathryn |
collection | PubMed |
description | S-nitrosation, commonly referred to as S-nitrosylation, is widely regarded as a ubiquitous, stable post-translational modification that directly regulates many proteins. Such a widespread role would appear to be incompatible with the inherent lability of the S-nitroso bond, especially its propensity to rapidly react with thiols to generate disulfide bonds. As anticipated, we observed robust and widespread protein S-nitrosation after exposing cells to nitrosocysteine or lipopolysaccharide. Proteins detected using the ascorbate-dependent biotin switch method are typically interpreted to be directly regulated by S-nitrosation. However, these S-nitrosated proteins are shown to predominantly comprise transient intermediates leading to disulfide bond formation. These disulfides are likely to be the dominant end effectors resulting from elevations in nitrosating cellular nitric oxide species. We propose that S-nitrosation primarily serves as a transient intermediate leading to disulfide formation. Overall, we conclude that the current widely held perception that stable S-nitrosation directly regulates the function of many proteins is significantly incorrect. |
format | Online Article Text |
id | pubmed-5807093 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Cell Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-58070932018-02-13 Evidence against Stable Protein S-Nitrosylation as a Widespread Mechanism of Post-translational Regulation Wolhuter, Kathryn Whitwell, Harry J. Switzer, Christopher H. Burgoyne, Joseph R. Timms, John F. Eaton, Philip Mol Cell Article S-nitrosation, commonly referred to as S-nitrosylation, is widely regarded as a ubiquitous, stable post-translational modification that directly regulates many proteins. Such a widespread role would appear to be incompatible with the inherent lability of the S-nitroso bond, especially its propensity to rapidly react with thiols to generate disulfide bonds. As anticipated, we observed robust and widespread protein S-nitrosation after exposing cells to nitrosocysteine or lipopolysaccharide. Proteins detected using the ascorbate-dependent biotin switch method are typically interpreted to be directly regulated by S-nitrosation. However, these S-nitrosated proteins are shown to predominantly comprise transient intermediates leading to disulfide bond formation. These disulfides are likely to be the dominant end effectors resulting from elevations in nitrosating cellular nitric oxide species. We propose that S-nitrosation primarily serves as a transient intermediate leading to disulfide formation. Overall, we conclude that the current widely held perception that stable S-nitrosation directly regulates the function of many proteins is significantly incorrect. Cell Press 2018-02-01 /pmc/articles/PMC5807093/ /pubmed/29358077 http://dx.doi.org/10.1016/j.molcel.2017.12.019 Text en © 2017 The Author(s) http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Wolhuter, Kathryn Whitwell, Harry J. Switzer, Christopher H. Burgoyne, Joseph R. Timms, John F. Eaton, Philip Evidence against Stable Protein S-Nitrosylation as a Widespread Mechanism of Post-translational Regulation |
title | Evidence against Stable Protein S-Nitrosylation as a Widespread Mechanism of Post-translational Regulation |
title_full | Evidence against Stable Protein S-Nitrosylation as a Widespread Mechanism of Post-translational Regulation |
title_fullStr | Evidence against Stable Protein S-Nitrosylation as a Widespread Mechanism of Post-translational Regulation |
title_full_unstemmed | Evidence against Stable Protein S-Nitrosylation as a Widespread Mechanism of Post-translational Regulation |
title_short | Evidence against Stable Protein S-Nitrosylation as a Widespread Mechanism of Post-translational Regulation |
title_sort | evidence against stable protein s-nitrosylation as a widespread mechanism of post-translational regulation |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5807093/ https://www.ncbi.nlm.nih.gov/pubmed/29358077 http://dx.doi.org/10.1016/j.molcel.2017.12.019 |
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