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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, Sigurlaug Sveinbjörnsdóttir, Rob M. A. de Bie, Jean-Marc Taymans, 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 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.