Parkin-associated Parkinson's disease

Rainer Von Coelln, Valina L. Dawson, Ted M. Dawson

Research output: Contribution to journalReview articlepeer-review

Abstract

Mutations in the PARK2 gene coding for parkin cause autosomal recessive juvenile parkinsonism (AR-JP), a familial form of Parkinson's disease (PD). Parkin functions as an E3 ubiquitin ligase, and loss of this ubiquitin ligase activity appears to be the mechanism underlying pathogenesis of AR-JP. Recently, the spectrum of genetic, clinical, and pathological findings on AR-JP has been significantly expanded. Moreover, a considerable number of parkin interactors and/or substrates have been identified and characterized, and animal models of parkin deficiency have been generated. In this review, we provide an overview of the most relevant findings and discuss their implications for the pathogenesis of AR-JP and sporadic PD.

Original languageEnglish (US)
Pages (from-to)175-184
Number of pages10
JournalCell and Tissue Research
Volume318
Issue number1
DOIs
StatePublished - Oct 1 2004

Keywords

  • Autosomal recessive juvenile parkinsonism
  • E3 ubiquitin ligase
  • PARK2
  • Parkin
  • Proteasome

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Histology
  • Cell Biology

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