Abstract
Background: One of the signaling mechanisms mediated by nitric oxide (NO) is through S-nitrosylation, the reversible redox-based modification of cysteine residues, on target proteins that regulate a myriad of physiological and pathophysiological processes. In particular, an increasing number of studies have identified important roles for S-nitrosylation in regulating cell death. Scope of review: The present review focuses on different targets and functional consequences associated with nitric oxide and protein S-nitrosylation during neuronal cell death. Major conclusions: S-Nitrosylation exhibits double-edged effects dependent on the levels, spatiotemporal distribution, and origins of NO in the brain: in general Snitrosylation resulting from the basal low level of NO in cells exerts anti-cell death effects, whereas S-nitrosylation elicited by induced NO upon stressed conditions is implicated in pro-cell death effects. General Significance: Dysregulated protein S-nitrosylation is implicated in the pathogenesis of several diseases including degenerative diseases of the central nervous system (CNS). Elucidating specific targets of S-nitrosylation as well as their regulatory mechanisms may aid in the development of therapeutic intervention in a wide range of brain diseases.
Original language | English (US) |
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Pages (from-to) | 736-742 |
Number of pages | 7 |
Journal | Biochimica et Biophysica Acta - General Subjects |
Volume | 1820 |
Issue number | 6 |
DOIs | |
State | Published - Jun 2012 |
Keywords
- Apoptosis
- Caspase
- GAPDH
- Nitric oxide
- S-nitrosylation
- XIAP
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology