一氧化氮通过对N-乙基马来酰亚胺敏感因子进行S-亚硝基化来调节胞吐作用。
Nitric oxide regulates exocytosis by S-nitrosylation of N-ethylmaleimide-sensitive factor.
作者信息
Matsushita Kenji, Morrell Craig N, Cambien Beatrice, Yang Shui Xiang, Yamakuchi Munekazu, Bao Clare, Hara Makoto R, Quick Richard A, Cao Wangsen, O'Rourke Brian, Lowenstein John M, Pevsner Jonathan, Wagner Denisa D, Lowenstein Charles J
机构信息
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
出版信息
Cell. 2003 Oct 17;115(2):139-50. doi: 10.1016/s0092-8674(03)00803-1.
Abstract
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, neurotransmission, thrombosis, and cytotoxic T lymphocyte cell killing.
摘要
一氧化氮（NO）可抑制血管炎症，但其抗炎特性的分子基础尚不清楚。我们发现，NO通过调节N-乙基马来酰亚胺敏感因子（NSF）的活性，抑制了魏贝尔-帕拉德小体（介导血管炎症和血栓形成的内皮颗粒）的胞吐作用。NO通过亚硝基化NSF的关键半胱氨酸残基，抑制NSF对可溶性NSF附着蛋白受体（SNARE）复合物进行解聚。NO可能在多种生理过程中调节胞吐作用，包括血管炎症、神经传递、血栓形成和细胞毒性T淋巴细胞杀伤。
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