Programmed cell death-2 isoform1 is ubiquitinated by parkin and increased in the substantia nigra of patients with autosomal recessive Parkinson’s disease
Name
Fukae-2009-Programmed cell deat.pdf
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Author(s)
Fukae, Jiro
Sato, Shigeto
Shiba, Kahori
Sato, Ken-ichi
Mori, Hideo
Mizuno, Yoshikuni
Hattori, Nobutaka
Sharp, Phillip A.
Date Issued
January 2009
Journal
FEBS Letters
Publisher
Elsevier
Citation
Fukae, Jiro, Shigeto Sato, Kahori Shiba, Ken-ichi Sato, Hideo Mori, Phillip A Sharp, Yoshikuni Mizuno, and Nobutaka Hattori. “Programmed Cell Death-2 Isoform1 Is Ubiquitinated by Parkin and Increased in the Substantia Nigra of Patients with Autosomal Recessive Parkinson’s Disease.” FEBS Letters 583, no. 3 (February 2009): 521–525. © 2009 Federation of European Biochemical Societies.
Version
Final published version
Abstract
Mutations in parkin gene are responsible for autosomal recessive Parkinson’s disease (ARPD) and its loss-of-function is assumed to affect parkin ubiquitin ligase activity. Accumulation of its substrate may induce dopaminergic neurodegeneration in the substantia nigra (SN) of ARPD. Here, we show that parkin interacts with programmed cell death-2 isoform 1 (PDCD2-1) and promotes its ubiquitination. Furthermore, accumulation of PDCD2-1 was found in the SN of ARPD as well as in sporadic PD, suggesting that common failure of the ubiquitin–proteasome system is associated with neuronal death in both ARPD and sporadic PD.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Koch Institute for Integrative Cancer Research at MIT
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Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
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DOI of Published Version
https://doi.org/10.1016/j.febslet.2008.12.055
