Biomol Ther 2018; 26(6): 533-538  https://doi.org/10.4062/biomolther.2018.179
Pathophysiological Role of S-Nitrosylation and Transnitrosylation Depending on S-Nitrosoglutathione Levels Regulated by S-Nitrosoglutathione Reductase
Min Sik Choi*
Lab of Pharmacology, College of Pharmacy, Dongduk Women’s University, Seoul 02748, Republic of Korea
E-mail: mschoi@dongduk.ac.kr
Tel: +82-2-940-4518, Fax: +82-2-940-4195
Received: September 18, 2018; Revised: September 27, 2018; Accepted: October 6, 2018; Published online: November 1, 2018.
© The Korean Society of Applied Pharmacology. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Nitric oxide (NO) mediates various physiological and pathological processes, including cell proliferation, differentiation, and inflammation. Protein S-nitrosylation (SNO), a NO-mediated reversible protein modification, leads to changes in the activity and function of target proteins. Recent findings on protein-protein transnitrosylation reactions (transfer of an NO group from one protein to another) have unveiled the mechanism of NO modulation of specific signaling pathways. The intracellular level of S-nitrosoglutathione (GSNO), a major reactive NO species, is controlled by GSNO reductase (GSNOR), a major regulator of NO/SNO signaling. Increasing number of GSNOR-related studies have shown the important role that denitrosylation plays in cellular NO/SNO homeostasis and human pathophysiology. This review introduces recent evidence of GSNO-mediated NO/SNO signaling depending on GSNOR expression or activity. In addition, the applicability of GSNOR as a target for drug therapy will be discussed in this review.
Keywords: Nitric Oxide, S-nitrosylation, Transnitrosylation, GSNO, GSNOR


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