共 131 条
Protein denitrosylation: enzymatic mechanisms and cellular functions
被引:405
作者:

Benhar, Moran
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机构: Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA

Forrester, Michael T.
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h-index: 0
机构: Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA

Stamler, Jonathan S.
论文数: 0 引用数: 0
h-index: 0
机构:
Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA
机构:
[1] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA
关键词:
NITRIC-OXIDE SYNTHASE;
S-NITROSOGLUTATHIONE REDUCTASE;
RED-BLOOD-CELLS;
AMYOTROPHIC-LATERAL-SCLEROSIS;
VASCULAR ENDOTHELIAL-CELLS;
NITROSATIVE STRESS;
SIGNAL-TRANSDUCTION;
DISULFIDE-ISOMERASE;
IN-VIVO;
NITROSOTHIOL FORMATION;
D O I:
10.1038/nrm2764
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
S-Nitrosylation, the redox-based modification of Cys thiol side chains by nitric oxide, is a common mechanism in signal transduction. Dysregulated S-nitrosylation contributes to a range of human pathologies. New roles for protein denitrosylation in regulating S-nitrosylation are being revealed. Recently, several denitrosylases - the enzymes that mediate Cys denitrosylation - have been discovered, of which two enzyme systems in particular, the S-nitrosoglutathione reductase and thioredoxin systems, have been shown to be physiologically relevant. These highly conserved enzymes regulate signalling through multiple classes of receptors and influence diverse cellular responses. In addition, they protect from nitrosative stress in microorganisms, mammals and plants, thereby exerting profound effects on host-microbe interactions and innate immunity.
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页码:721 / 732
页数:12
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