| S-nitrosylation in cardiovascular signaling. | |
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MedLine Citation:
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PMID: 20203313 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Well over 2 decades have passed since the endothelium-derived relaxation factor was reported to be the gaseous molecule nitric oxide (NO). Although soluble guanylyl cyclase (which generates cyclic guanosine monophosphate, cGMP) was the first identified receptor for NO, it has become increasingly clear that NO exerts a ubiquitous influence in a cGMP-independent manner. In particular, many, if not most, effects of NO are mediated by S-nitrosylation, the covalent modification of a protein cysteine thiol by an NO group to generate an S-nitrosothiol (SNO). Moreover, within the current framework of NO biology, endothelium-derived relaxation factor activity (ie, G protein-coupled receptor-mediated, or shear-induced endothelium-derived NO bioactivity) is understood to involve a central role for SNOs, acting both as second messengers and signal effectors. Furthermore, essential roles for S-nitrosylation have been implicated in virtually all major functions of NO in the cardiovascular system. Here, we review the basic biochemistry of S-nitrosylation (and denitrosylation), discuss the role of S-nitrosylation in the vascular and cardiac functions of NO, and identify current and potential clinical applications. |
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Authors:
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Brian Lima; Michael T Forrester; Douglas T Hess; Jonathan S Stamler |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review |
Journal Detail:
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Title: Circulation research Volume: 106 ISSN: 1524-4571 ISO Abbreviation: Circ. Res. Publication Date: 2010 Mar |
Date Detail:
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Created Date: 2010-03-05 Completed Date: 2010-03-26 Revised Date: 2011-07-26 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: United States |
Other Details:
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Languages: eng Pagination: 633-46 Citation Subset: IM |
Affiliation:
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Department of Surgery, Duke University Medical Center, Durham, NC, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis Cardiovascular Diseases / metabolism*, pathology, physiopathology Cardiovascular System / metabolism*, pathology, physiopathology Cyclic GMP / metabolism Endothelium, Vascular / metabolism Endothelium-Dependent Relaxing Factors / metabolism Humans Inflammation / metabolism Myocardium / metabolism Neovascularization, Physiologic Nitric Oxide / metabolism* Protein Processing, Post-Translational* S-Nitrosothiols / metabolism* Signal Transduction* Vascular Resistance |
| Grant Support | |
ID/Acronym/Agency:
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P01 HL075443-050003/HL/NHLBI NIH HHS; P01-HL075443/HL/NHLBI NIH HHS; R01 HL059130-11/HL/NHLBI NIH HHS; R01 HL091876-01A1/HL/NHLBI NIH HHS; R01 HL095463/HL/NHLBI NIH HHS; R01 HL095463-01A1/HL/NHLBI NIH HHS; R01 HL096673-01/HL/NHLBI NIH HHS; R01-HL059130/HL/NHLBI NIH HHS; R01-HL091876/HL/NHLBI NIH HHS; R01-HL096673/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Endothelium-Dependent Relaxing Factors; 0/S-Nitrosothiols; 10102-43-9/Nitric Oxide; 7665-99-8/Cyclic GMP |
| Comments/Corrections | |
Comment In:
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Circ Res. 2010 Jul 9;107(1):e1; author reply e2-3
[PMID:
20616330
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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