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Dynamic and redundant regulation of LRRK2 and LRRK1 expression
Authors:Saskia Biskup  Darren J Moore  Alexis Rea  Bettina Lorenz-Deperieux  Candice E Coombes  Valina L Dawson  Ted M Dawson  Andrew B West
Institution:(1) Institute for Cell Engineering and Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, USA;(2) Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, USA;(3) Institute of Human Genetics, GSF National Research Center for Environment and Health, Munich, Neuherberg, Germany;(4) Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, USA;(5) Center for Neurodegeneration and Experimental Therapeutics and Department of Neurology, University of Alabama at Birmingham, Birmingham, USA
Abstract:

Background  

Mutations within the leucine-rich repeat kinase 2 (LRRK2) gene account for a significant proportion of autosomal-dominant and some late-onset sporadic Parkinson's disease. Elucidation of LRRK2 protein function in health and disease provides an opportunity for deciphering molecular pathways important in neurodegeneration. In mammals, LRRK1 and LRRK2 protein comprise a unique family encoding a GTPase domain that controls intrinsic kinase activity. The expression profiles of the murine LRRK proteins have not been fully described and insufficiently characterized antibodies have produced conflicting results in the literature.
Keywords:
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