학술논문
Insights into the cellular consequences of LRRK2-mediated Rab protein phosphorylation.
Document Type
Article
Source
Subject
*PARKINSON'S disease
*PHOSPHORYLATION
*
Language
ISSN
0300-5127
Abstract
Point mutations in leucine-rich repeat kinase 2 (LRRK2) which cause Parkinson's disease increase its kinase activity, and a subset of Rab GTPases have been identified as endogenous LRRK2 kinase substrates. Their phosphorylation correlates with a loss-offunction for the membrane trafficking steps they are normally involved in, but it also allows them to bind to a novel set of effector proteins with dominant cellular consequences. In this brief review, we will summarize novel findings related to the LRRK2-mediated phosphorylation of Rab GTPases and its various cellular consequences in vitro and in the intact brain, and we will highlight major outstanding questions in the field. [ABSTRACT FROM AUTHOR]