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Beilina, A.* ; Rudenko, I.N.* ; Kaganovich, A.* ; Civiero, L.* ; Chau, H.* ; Kalia, S.K.* ; Kalia, L.V.* ; Lobbestael, E.* ; Chia, R.* ; Ndukwe, K.* ; Ding, J.* ; Nalls, M.A.* ; EUMODIC Consortium (Illig, T. ; Lichtner, P. ; *) ; Olszewski, M.* ; Hauser, D.N.* ; Kumaran, R.* ; Lozano, A.M.* ; Baekelandt, V.* ; Greene, L.E.* ; Taymans, J.-M.* ; Greggio, E.* ; Cookson, M.R.*

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

Proc. Natl. Acad. Sci. U.S.A. 111, 2626-2631 (2014)
DOI
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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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
ISSN (print) / ISBN 0027-8424
e-ISSN 1091-6490
Journal Proceedings of the National Academy of Sciences of the United States of America
Quellenangaben Volume: 111, Issue: 7, Pages: 2626-2631 Article Number: , Supplement: ,
Publisher National Academy of Sciences
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Epidemiology II (EPI2)