Sulfhydration mediates neuroprotective actions of parkin

M. Scott Vandiver, Bindu D. Paul, Risheng Xu, Senthilkumar Karuppagounder, Feng Rao, Adele M. Snowman, Han Seok Ko, Yun Il Lee, Valina L. Dawson, Ted M. Dawson, Nilkantha Sen and Solomon H. Snyder ()
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M. Scott Vandiver: Johns Hopkins University School of Medicine
Bindu D. Paul: Johns Hopkins University School of Medicine
Risheng Xu: Johns Hopkins University School of Medicine
Senthilkumar Karuppagounder: Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine
Feng Rao: Johns Hopkins University School of Medicine
Adele M. Snowman: Johns Hopkins University School of Medicine
Han Seok Ko: Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine
Yun Il Lee: Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine
Valina L. Dawson: Johns Hopkins University School of Medicine
Ted M. Dawson: Johns Hopkins University School of Medicine
Nilkantha Sen: Johns Hopkins University School of Medicine
Solomon H. Snyder: Johns Hopkins University School of Medicine

Nature Communications, 2013, vol. 4, issue 1, 1-7

Abstract: Abstract 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.

Date: 2013
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DOI: 10.1038/ncomms2623

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