The role of parkin in familial and sporadic Parkinson's disease

Authors

  • Ted M. Dawson MD, PhD,

    Corresponding author
    1. Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    2. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    3. Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    • Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, 733 North Broadway, BRB 731, Baltimore, MD 21205
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  • Valina L. Dawson PhD

    1. Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    2. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    3. Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    4. Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
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  • Potential conflict of interest: Nothing to report.

Abstract

Mutations in parkin are the second most common known cause of Parkinson's disease (PD). Parkin is an ubiquitin E3 ligase that monoubiquitinates and polyubiquitinates proteins to regulate a variety of cellular processes. Loss of parkin's E3 ligase activity is thought to play a pathogenic role in both inherited and sporadic PD. Here, we review parkin biology and pathobiology and its role in the pathogenesis of PD. © 2010 Movement Disorder Society

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