Journal
NITRIC OXIDE-BIOLOGY AND CHEMISTRY
Volume 42, Issue -, Pages 9-18Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.niox.2014.07.002
Keywords
Nitrosation; S-nitrosylation; Apoptosis; Cell death; Survival; Cancer
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Funding
- NATIONAL CANCER INSTITUTE [SC1CA173069] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [SC1HL112630] Funding Source: NIH RePORTER
- NCI NIH HHS [SC1 CA173069] Funding Source: Medline
- NHLBI NIH HHS [SC1 HL112630] Funding Source: Medline
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Nitric oxide, a reactive free radical, is an important signaling molecule that can lead to a plethora of cellular effects affecting homeostasis. A well-established mechanism by which NO manifests its effect on cellular functions is the post-translational chemical modification of cysteine thiols in substrate proteins by a process known as S-nitrosation. Studies that investigate regulation of cellular functions through NO have increasingly established S-nitrosation as the primary modulatory mechanism in their respective systems. There has been a substantial increase in the number of reports citing various candidate proteins undergoing S-nitrosation, which affects cell-death and -survival pathways in a number of tissues including heart, lung, brain and blood. With an exponentially growing list of proteins being identified as substrates for S-nitrosation, it is important to assimilate this information in different cell/tissue systems in order to gain an overall view of protein regulation of both individual proteins and a class of protein substrates. This will allow for broad mapping of proteins as a function of S-nitrosation, and help delineate their global effects on pathophysiological responses including cell death and survival. This information will not only provide a much better understanding of overall functional relevance of NO in the context of various disease states, it will also facilitate the generation of novel therapeutics to combat specific diseases that are driven by NO-mediated S-nitrosation. (C) 2014 Elsevier Inc. All rights reserved.
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