Nitric oxide regulates exocytosis by S-nitrosylation of N-ethylmaleimdide-sensitive factor

被引：364

作者：

Matsushita, K

Morrell, CN

Cambien, B

Yang, SX

Yamakuchi, M

Bao, C

Hara, MR

Quick, RA

Cao, W

O'Rourke, B

Lowenstein, JM

Pevsner, J

Wagner, DD

Lowenstein, CJ ^{[1
]}

机构：

[1] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA

[2] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA

[3] Johns Hopkins Univ, Sch Med, Dept Comparat Med, Baltimore, MD 21205 USA

[4] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA

[5] Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, Baltimore, MD 21205 USA

[6] Brandeis Univ, Dept Biochem, Waltham, MA 02454 USA

[7] Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA

[8] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA

来源：

CELL | 2003年 / 115卷 / 02期

关键词：

D O I：

10.1016/S0092-8674(03)00803-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Nitric oxide (NO) inhibits vascular inflammation, but the molecular basis for its anti-inflammatory properties is unknown. We show that NO inhibits exocytosis of Weibel-Palade bodies, endothelial granules that mediate vascular inflammation and thrombosis, by regulating the activity of N-ethylmaleimide-sensitive factor (NSF). NO inhibits NSF disassembly of soluble NSF attachment protein receptor (SNARE) complexes by nitrosylating critical cysteine residues of NSF. NO may regulate exocytosis in a variety of physiological processes, including vascular inflammation, neuro-transmission, thrombosis, and cytotoxic T lymphocyte cell killing.

引用

页码：139 / 150

页数：12

共 52 条

[1] Platelets adhere to and translocate on von Willebrand factor presented by endothelium in simulated veins [J].