| Literature DB >> 24440455 |
Elizabeth Murphy1, Mark Kohr2, Sara Menazza3, Tiffany Nguyen3, Alicia Evangelista3, Junhui Sun3, Charles Steenbergen4.
Abstract
Nitric oxide is a gaseous signaling molecule that is well-known for the Nobel prize-winning research that defined nitric oxide as a physiological regulator of blood pressure in the cardiovascular system. Nitric oxide can signal via the classical pathway involving activation of guanylyl cyclase or by a post-translational modification, referred to as S-nitrosylation (SNO) that can occur on cysteine residues of proteins. As proteins with cysteine residues are common, this allows for amplification of the nitric oxide signaling. This review will focus on the possible mechanisms through which SNO can alter protein function in cardiac cells, and the role of SNO occupancy in these mechanisms. The specific mechanisms that regulate protein SNO, including redox-dependent processes, will also be discussed. This article is part of a Special Issue entitled "Redox Signalling in the Cardiovascular System". Published by Elsevier Ltd.Entities:
Keywords: Cardioportection; Nitric oxide; Oxidation
Mesh:
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Year: 2014 PMID: 24440455 PMCID: PMC4214076 DOI: 10.1016/j.yjmcc.2014.01.003
Source DB: PubMed Journal: J Mol Cell Cardiol ISSN: 0022-2828 Impact factor: 5.000