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Sulfhydration mediates neuroprotective actions of parkin

Author

Listed:
  • 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
    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
    Johns Hopkins University School of Medicine)

  • Yun Il Lee

    (Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine
    Johns Hopkins University School of Medicine)

  • Valina L. Dawson

    (Johns Hopkins University School of Medicine
    Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine
    Johns Hopkins University School of Medicine
    Johns Hopkins University School of Medicine)

  • Ted M. Dawson

    (Johns Hopkins University School of Medicine
    Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine
    Johns Hopkins University School of Medicine)

  • Nilkantha Sen

    (Johns Hopkins University School of Medicine
    Institute of Molecular Medicine and Genetics, Medical College of Georgia)

  • Solomon H. Snyder

    (Johns Hopkins University School of Medicine
    Johns Hopkins University School of Medicine
    Johns Hopkins University School of Medicine)

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.

Suggested Citation

  • 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 & Solomon H. Sn, 2013. "Sulfhydration mediates neuroprotective actions of parkin," Nature Communications, Nature, vol. 4(1), pages 1-7, June.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms2623
    DOI: 10.1038/ncomms2623
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