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Unbiased screen for interactors of leucine-rich repeat kinase 2 supports a common pathway for sporadic and familial Parkinson disease.

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Authors
Beilina, Alexandria
Rudenko, Iakov N
Kaganovich, Alice
Civiero, Laura
Chau, Hien
Kalia, Suneil K
Kalia, Lorraine V
Lobbestael, Evy
Chia, Ruth
Ndukwe, Kelechi
Ding, Jinhui
Nalls, Mike A
Olszewski, Maciej
Hauser, David N
Kumaran, Ravindran
Lozano, Andres M
Baekelandt, Veerle
Greene, Lois E
Taymans, Jean-Marc
Greggio, Elisa
Cookson, Mark R
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Issue Date
2014-02-18

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Citation
Proc. Natl. Acad. Sci. U.S.A. 2014, 111 (7):2626-31
Abstract
Mutations in leucine-rich repeat kinase 2 (LRRK2) cause inherited Parkinson disease (PD), and common variants around LRRK2 are a risk factor for sporadic PD. Using protein-protein interaction arrays, we identified BCL2-associated athanogene 5, Rab7L1 (RAB7, member RAS oncogene family-like 1), and Cyclin-G-associated kinase as binding partners of LRRK2. The latter two genes are candidate genes for risk for sporadic PD identified by genome-wide association studies. These proteins form a complex that promotes clearance of Golgi-derived vesicles through the autophagy-lysosome system both in vitro and in vivo. We propose that three different genes for PD have a common biological function. More generally, data integration from multiple unbiased screens can provide insight into human disease mechanisms.
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To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Files. This article is open access.
Additional Links
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3932908/
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Archived with thanks to Proceedings of the National Academy of Sciences of the United States of America
ae974a485f413a2113503eed53cd6c53
10.1073/pnas.1318306111
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