Volume 25, Issue S1 p. S32-S39
Pathogenesis and Implications for Neuroprotection

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

Ted M. Dawson MD, PhD

Corresponding Author

Ted M. Dawson MD, PhD

Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

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 21205Search for more papers by this author
Valina L. Dawson PhD

Valina L. Dawson PhD

Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

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First published: 25 February 2010
Citations: 298

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