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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

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

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.[1]

References

  1. Nitric oxide regulates exocytosis by S-nitrosylation of N-ethylmaleimide-sensitive factor. Matsushita, K., Morrell, C.N., Cambien, B., Yang, S.X., Yamakuchi, M., Bao, C., Hara, M.R., Quick, R.A., Cao, W., O'Rourke, B., Lowenstein, J.M., Pevsner, J., Wagner, D.D., Lowenstein, C.J. Cell (2003) [Pubmed]
 
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