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H2S Signals Through Protein S-Sulfhydration

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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.

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Patent

Fluorescent probes for reactive sulfur species

TL;DR: In this paper, reaction-based fluorescent probes for selective imaging of hydrogen sulfide in living cells were proposed, which can be used to detect the presence of hydrogen in living organisms.
Journal ArticleDOI

Sp1 S-Sulfhydration Induced by Hydrogen Sulfide Inhibits Inflammation via HDAC6/MyD88/NF-κB Signaling Pathway in Adjuvant-Induced Arthritis

TL;DR: It is shown that HDAC6 protein level was increased in the synovium tissues of adjuvant-induced arthritis rats and hydrogen sulfide (H2S) donor S-propargyl-cysteine (SPRC) can inhibitHDAC6 expression and alleviate inflammatory response in vivo, and S-sulfhydration of Sp1 by antioxidant molecular H2S ameliorates RA progression via the HDAC 6/MyD88/NF-κB signaling pathway
BookDOI

Mitochondria in Skeletal Muscle Health, Aging and Diseases

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Regulation of Aqueous Humor Dynamics by Hydrogen Sulfide: Potential Role in Glaucoma Pharmacotherapy.

TL;DR: Exogenous application of H2S-releasing compounds was reported to increase aqueous humor outflow facility in an ex vivo model of the porcine ocular anterior segment and lowered intraocular pressure (IOP) in both normotensive and glaucomatous rabbits.
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Gasotransmitters for the Therapeutic Prevention of Hypertension and Kidney Disease

TL;DR: In this paper, the authors summarized the current evidence of gasotransmitter-based interventions for prevention of hypertension and kidney disease in animal models, highlighting their key roles in hypertension and renal disease.
References
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Journal ArticleDOI

H2S as a Physiologic Vasorelaxant: Hypertension in Mice with Deletion of Cystathionine γ-Lyase

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.

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.

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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