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Molecular & Cellular Proteomics 5:1193-1204, 2006.
© 2006 by The American Society for Biochemistry and Molecular Biology, Inc.

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Research

Proteomic Identification of a Stress Protein, Mortalin/mthsp70/GRP75

Relevance To Parkinson Disease^*,S

Jinghua Jin, Christine Hulette, Yan Wang, Terry Zhang^¶, Catherine Pan, Renu Wadhwa^|| and Jing Zhang^,

From the Department of Pathology, University of Washington School of Medicine, Seattle, Washington 98104, Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, ^¶ Thermo Electron Corporation, San Jose, California 95134, and ^|| Gene Function Research Center, National Institute of Advanced Industrial Science and Technology, 1-1-1 Higashi, Tsukuba Science City 305-8562, Japan

Functional impairment of mitochondria and proteasomes and increased oxidative damage comprise the main pathological phenotypes of Parkinson disease (PD). Using an unbiased quantitative proteomic approach, we compared nigral mitochondrial proteins of PD patients with those from age-matched controls. 119 of 842 identified proteins displayed significant differences in their relative abundance (increase/decrease) between the two groups. We confirmed that one of these, mortalin (mthsp70/GRP75, a mitochondrial stress protein), is substantially decreased in PD brains as well as in a cellular model of PD. In addition, nine candidate mortalin-binding partners were identified as potential mediators of PD pathology. Manipulations of mortalin level in dopaminergic neurons resulted in significant changes in sensitivity to PD phenotypes via pathways involving mitochondrial and proteasomal function as well as oxidative stress.

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