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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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Hydrogen Sulfide Regulates Homeostasis of Mesenchymal Stem Cells and Regulatory T Cells

TL;DR: Current emerging evidence that H2S regulates mesenchymal stem cell and T-cell functions is discussed, and the authors discuss the growing number of diverse targets for which H2s serves as a gasotransmitter.
Journal ArticleDOI

S-glutathionylation of ion channels: insights into the regulation of channel functions, thiol modification crosstalk, and mechanosensing.

TL;DR: This review discusses S-glutathionylation-mediated structural and functional changes of ion channels, and thiol modification crosstalk, which could be a critical post-translational modification mechanism that regulates many molecules under oxidative stress.
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Quantitative determination of polysulfide in albumins, plasma proteins and biological fluid samples using a novel combined assays approach

TL;DR: A novel combined detection assay developed by modifying Sulfide Antioxidant Buffer to produce an "Elimination Method of Sulfides from Polysulfide" (EMSP) treatment solution that liberates sulfide, followed with methylene blue (MB) sulfide detection assay revealed that serum albumin is a major pool of polysulfides in human blood circulation, suggesting that sulfide was released from low molecular weight sulfur species.
Journal ArticleDOI

Quantitative and comparative liquid chromatography-electrospray ionization-mass spectrometry analyses of hydrogen sulfide and thiol metabolites derivaitized with 2-iodoacetanilide isotopologues

TL;DR: A new method for quantitative analyses of H2S and thiol metabolites using the procedure of pre-column 2-IAN derivatization coupled with liquid chromatography-electrospray ionization-mass spectrometry (LC-ESI-MS) to achieve quantitative and matched sample comparative analyses with minimal bias is proposed.
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Hydrogen Sulfide Therapy in Diabetes-Accelerated Atherosclerosis: A Whiff of Success.

TL;DR: Although long considered a toxic gas, studies in the past decade have revealed important physiological roles for H2S, which exerts potent antioxidant, antiapoptotic, anti-inflammatory, and angiogenic responses in patients with diabetes.
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.
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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