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Cardiovascular Research 2007 75(2):229-239; doi:10.1016/j.cardiores.2007.04.013
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Copyright © 2007, European Society of Cardiology

Nitric oxide cell signaling: S-nitrosation of Ras superfamily GTPases

Kimberly W. Rainesa,b, Marcelo G. Boninic and Sharon L. Campbella,b,*

aDepartment of Biochemistry and Biophysics, University of North Carolina, 530 Mary Ellen Jones Building, Chapel Hill, NC 27599-7260, United States
bLineberger Comprehensive Cancer Center, University of North Carolina, 530 Mary Ellen Jones Building, Chapel Hill, NC 27599-7260, United States
cLaboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, United States

* Corresponding author. Lineberger Comprehensive Cancer Center, University of North Carolina, 530 Mary Ellen Jones Building, Chapel Hill, NC 27599-7260, United States. Tel.: +1 919 966 7139; fax: +1 919 966 2852. campbesl{at}med.unc.edu

The Ras superfamily of small GTPases cycle between inactive GDP-bound and active GTP-bound states to modulate a diverse array of processes involved in cellular growth control. While the basic mechanisms by which GTPase regulatory proteins regulate GTPase substrates have been revealed through numerous studies, detailed studies into the mechanism(s) of free radical-mediated GTPase regulation have only more recently been tackled. This article reviews the mechanism of free radical-mediated GTPase regulation and shows nitric oxide can serve as important regulator of small GTPase proteins (i.e. Ras and RhoA) through protein modifications such as S-nitrosation.

KEYWORDS Nitric oxide; Redox signaling; Small GTPases


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