| First Author | Okamoto S | Year | 2015 |
| Journal | Biochim Biophys Acta | Volume | 1850 |
| Issue | 8 | Pages | 1588-93 |
| PubMed ID | 25527866 | Mgi Jnum | J:253938 |
| Mgi Id | MGI:6100260 | Doi | 10.1016/j.bbagen.2014.12.013 |
| Citation | Okamoto S, et al. (2015) S-Nitrosylation in neurogenesis and neuronal development. Biochim Biophys Acta 1850(8):1588-93 |
| abstractText | BACKGROUND: Nitric oxide (NO) is a pleiotropic messenger molecule. The multidimensional actions of NO species are, in part, mediated by their redox nature. Oxidative posttranslational modification of cysteine residues to regulate protein function, termed S-nitrosylation, constitutes a major form of redox-based signaling by NO. SCOPE OF REVIEW: S-Nitrosylation directly modifies a number of cytoplasmic and nuclear proteins in neurons. S-Nitrosylation modulates neuronal development by reaction with specific proteins, including the transcription factor MEF2. This review focuses on the impact of S-nitrosylation on neurogenesis and neuronal development. MAJOR CONCLUSIONS: Functional characterization of S-nitrosylated proteins that regulate neuronal development represents a rapidly emerging field. Recent studies reveal that S-nitrosylation-mediated redox signaling plays an important role in several biological processes essential for neuronal differentiation and maturation. GENERAL SIGNIFICANCE: Investigation of S-nitrosylation in the nervous system has elucidated new molecular and cellular mechanisms for neuronal development. S-Nitrosylated proteins in signaling networks modulate key events in brain development. Dysregulation of this redox-signaling pathway may contribute to neurodevelopmental disabilities such as autism spectrum disorder (ASD). Thus, further elucidation of the involvement of S-nitrosylation in brain development may offer potential therapeutic avenues for neurodevelopmental disorders. This article is part of a Special Issue entitled Redox regulation of differentiation and de-differentiation. |
