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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...

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Autores principales: Wolhuter, Kathryn, Whitwell, Harry J., Switzer, Christopher H., Burgoyne, Joseph R., Timms, John F., Eaton, Philip
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cell Press 2018
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.
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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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