The role of parkin in familial and sporadic Parkinson's disease†
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 authorValina 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
Search for more papers by this authorCorresponding 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 authorValina 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
Search for more papers by this authorPotential 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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