Pathophysiological Role of S-Nitrosylation and Transnitrosylation Depending on S-Nitrosoglutathione Levels Regulated by S-Nitrosoglutathione Reductase
Biomolecules & Therapeutics
; : 533-538, 2018.
Article
in En
| WPRIM
| ID: wpr-717961
Responsible library:
WPRO
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.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Oxidoreductases
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Pathologic Processes
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S-Nitrosoglutathione
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Cell Proliferation
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Drug Therapy
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Homeostasis
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Inflammation
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Nitric Oxide
Limits:
Humans
Language:
En
Journal:
Biomolecules & Therapeutics
Year:
2018
Type:
Article