帕金
神经保护
帕金森病
S-亚硝基化
化学
硫化氢
泛素
突变
泛素连接酶
机制(生物学)
生物化学
疾病
药理学
生物
医学
突变
半胱氨酸
酶
基因
内科学
有机化学
硫黄
哲学
认识论
作者
M. Scott Vandiver,Bindu D. Paul,Risheng Xu,Senthilkumar S. Karuppagounder,Feng Rao,Adele M. Snowman,Han Seok Ko,Yun-Il Lee,Valina L. Dawson,Ted M. Dawson,Nilkantha Sen,Solomon H. Snyder
摘要
Increases in S-nitrosylation and inactivation of the neuroprotective ubiquitin E3 ligase, parkin, in the brains of patients with Parkinson's disease are thought to be pathogenic and suggest a possible mechanism linking parkin to sporadic Parkinson's disease. Here we demonstrate that physiologic modification of parkin by hydrogen sulfide, termed sulfhydration, enhances its catalytic activity. Sulfhydration sites are identified by mass spectrometry analysis and are investigated by site-directed mutagenesis. Parkin sulfhydration is markedly depleted in the brains of patients with Parkinson's disease, suggesting that this loss may be pathologic. This implies that hydrogen sulfide donors may be therapeutic.
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