H2S Signals Through Protein S-Sulfhydration
Asif K. Mustafa,Moataz M. Gadalla,Nilkantha Sen,Seyun Kim,Weitong Mu,Sadia K. Gazi,Roxanne K. Barrow,Guangdong Yang,Rui Wang,Solomon H. Snyder +9 more
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TLDR
Ex vivo endogenous H2S physiologically modifies cysteine residues in many proteins, including glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and actin, converting Cysteine -SH groups to -SSH groups in a process the authors call S-sulfhydration.Abstract:
Hydrogen sulfide (H2S), a messenger molecule generated by cystathionine gamma-lyase, acts as a physiologic vasorelaxant. Mechanisms whereby H2S signals have been elusive. We now show that H2S physiologically modifies cysteines in a large number of proteins by S-sulfhydration. About 10 to 25% of many liver proteins, including actin, tubulin, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), are sulfhydrated under physiological conditions. Sulfhydration augments GAPDH activity and enhances actin polymerization. Sulfhydration thus appears to be a physiologic posttranslational modification for proteins.read more
Citations
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Journal ArticleDOI
Chemical methods to detect S-nitrosation.
TL;DR: A focus is on the methods which can be used to directly conjugate the site(s) of S-nitrosation, which represents an important post-translational modification that transduces NO-dependent signals.
Journal ArticleDOI
CoQ deficiency causes disruption of mitochondrial sulfide oxidation, a new pathomechanism associated with this syndrome
Marta Luna-Sánchez,Agustín Hidalgo-Gutiérrez,Tatjana M. Hildebrandt,Julio Chaves-Serrano,Eliana Barriocanal-Casado,Ángela Santos-Fandila,Miguel Romero,Ramy K. A. Sayed,Ramy K. A. Sayed,Juan Duarte,Holger Prokisch,Markus Schuelke,Felix Distelmaier,Germaine Escames,Darío Acuña-Castroviejo,Luis C. López +15 more
TL;DR: It is demonstrated that severe CoQ deficiency causes a reduction in SQR levels and activity, which leads to an alteration of mitochondrial sulfide metabolism and the blood pressure is reduced.
Journal ArticleDOI
Hydrogen sulfide-induced vasodilation mediated by endothelial TRPV4 channels.
TL;DR: Results demonstrate that H2S-mediated vasodilation involves activation of TRPV4-dependent Ca2+ influx and BK channel activation within EC, which appears to cause calcium events that result in the opening of eBK channels, endothelial hyperpolarization, and subsequent vasodillation.
Journal ArticleDOI
Hydrogen sulfide regulates cardiac mitochondrial biogenesis via the activation of AMPK
Yuuki Shimizu,Rohini Polavarapu,Kattri-Liis Eskla,Chad K. Nicholson,Christopher A. Koczor,Rui Wang,William Lewis,Sruti Shiva,David J. Lefer,John W. Calvert +9 more
TL;DR: It is found that restoring H2S levels with SG-1002 in the setting of heart failure increased cardiac mitochondrial content, improved mitochondrial respiration, improved ATP production efficiency, and improved cardiac function.
Book ChapterDOI
Chapter Five – Protein Sulfhydration
Bindu D. Paul,Solomon H. Snyder +1 more
TL;DR: The biotin switch assay, originally developed to detect nitrosylation, has been modified to detect sulfhydration and the methodologies used to detect this modification are discussed.
References
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Journal ArticleDOI
H2S as a Physiologic Vasorelaxant: Hypertension in Mice with Deletion of Cystathionine γ-Lyase
Guangdong Yang,Guangdong Yang,Lingyun Wu,Bo Jiang,Wei Yang,Jiansong Qi,Kun Cao,Qinghe Meng,Asif K. Mustafa,Weitong Mu,Shengming Zhang,Solomon H. Snyder,Rui Wang,Rui Wang +13 more
TL;DR: It is shown that H2S is physiologically generated by cystathionine γ-lyase (CSE) and that genetic deletion of this enzyme in mice markedly reduces H 2S levels in the serum, heart, aorta, and other tissues.
Journal ArticleDOI
Protein S-nitrosylation: purview and parameters.
Douglas T. Hess,Akio Matsumoto,Sung Oog Kim,Harvey E. Marshall,Jonathan S. Stamler,Jonathan S. Stamler +5 more
TL;DR: S-nitrosylation conveys a large part of the ubiquitous influence of nitric oxide on cellular signal transduction, and provides a mechanism for redox-based physiological regulation.
Journal ArticleDOI
The vasorelaxant effect of H2S as a novel endogenous gaseous KATP channel opener
TL;DR: It is demonstrated that H2S is an important endogenous vasoactive factor and the first identified gaseous opener of KATP channels in vascular SMCs and production from vascular tissues was enhanced by nitric oxide.
Journal ArticleDOI
Hydrogen sulphide and its therapeutic potential
TL;DR: The physiology and biochemistry of H2S is overviews, the effects of H 2S inhibitors or H2s donors in animal models of disease are summarized, the potential options for the therapeutic exploitation of H1S are outlined and they are outlined.
Journal ArticleDOI
Protein S-nitrosylation: a physiological signal for neuronal nitric oxide.
Samie R. Jaffrey,Hediye Erdjument-Bromage,Christopher D. Ferris,Paul Tempst,Solomon H. Snyder +4 more
TL;DR: Protein S-nitrosylation is established as a physiological signalling mechanism for neuronally generated NO in mice harbouring a genomic deletion of neuronal NO synthase (nNOS).
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