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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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Clinical Use of Hydrogen Sulfide to Protect Against Intimal Hyperplasia

TL;DR: This review summarizes IH pathophysiology and treatment, and provides an overview of the potential clinical role of H2S to prevent IH and restenosis.

Development of Bacterial Quorum Sensing Inhibitors and Molecular Probes

Hanjing Peng
TL;DR: H2S has been recognized as an important gas‐ otransmitter and its concentration is relevant to a variety of diseases and a novel fluorescent probe has been developed for quantitation of H2S in aqueous solutions.
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Sulfane Sulfur Posttranslationally Modifies the Global Regulator AdpA to Influence Actinorhodin Production and Morphological Differentiation of Streptomyces coelicolor

TL;DR: Sulfane sulfur posttranslationally modifies AdPA in Streptomyces coelicolor via specifically reacting with Cys62 of AdpA to form a persulfide (Cys62-SSH) and this finding provides a new strategy for mining and activating valuable biosynthetic gene clusters.
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Hydrogen sulfide mediated the melatonin induced stoma closure by regulating the K+ channel in Arabidopsis thaliana

TL;DR: The role of the gasotransmitter hydrogen sulfide (H2S) and the phytohormone melatonin (MEL) in enhancing plant drought resistance are increasingly understood, but the specific regulatory mechanisms in response to drought remain unclear as mentioned in this paper .
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.
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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.
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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.
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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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