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, AlexandriaRudenko, 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
Issue Date
2014-02-18
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Proc. Natl. Acad. Sci. U.S.A. 2014, 111 (7):2626-31Abstract
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.Description
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3932908/Rights
Archived with thanks to Proceedings of the National Academy of Sciences of the United States of Americaae974a485f413a2113503eed53cd6c53
10.1073/pnas.1318306111
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