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National Academy of Sciences, Proceedings of the National Academy of Sciences, 7(111), p. 2626-2631, 2014

DOI: 10.1073/pnas.1318306111

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

Journal article published in 2014 by B. P. C. van de Warrenburg, Rob M. A. de Bie, Karin D. van Dijk, Jacobus J. van Hilten, François Tison, Daniah Trabzuni, Bart van de Warrenburg, André G. Uitterlinden, Mirdhu Wickremaratchi, Daan Velseboer, Nigel Williams, Caroline H. Williams-Gray, Marie Vidailhet, Robert Walker, Sophie Winder-Rhodes and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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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.