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The role of (auto)-phosphorylation in the complex activation mechanism of LRRK2

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dc.creator Athanasopoulos, Panagiotis S.
dc.creator Heumann, Rolf
dc.creator Kortholt, Arjan
dc.date 2018-07-01T00:00:00Z
dc.date.accessioned 2023-01-09T12:02:33Z
dc.date.available 2023-01-09T12:02:33Z
dc.identifier 4e60dbd1-fd5a-487d-9e82-c126ca2abddd
dc.identifier 10.1515/hsz-2017-0332
dc.identifier https://avesis.sdu.edu.tr/publication/details/4e60dbd1-fd5a-487d-9e82-c126ca2abddd/oai
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/97833
dc.description Mutations in human leucine-rich-repeat kinase 2 (LRRK2) have been found to be the most frequent cause of late-onset Parkinson's Disease (PD). LRRK2 is a large protein with two enzymatic domains, a GTPase and a kinase domain. A cluster of (auto)-phosphorylation sites within the N-terminus of LRRK2 have been shown to be crucial for the localization of LRRK2 and is important for PD pathogenesis. In addition, phosphorylation of sites within the G-domain of the protein affect GTPase activity. Here we discuss the role of these (auto)-phosphorylation sites of LRRK2 and their regulation by phosphatases and upstream kinases.
dc.language eng
dc.rights info:eu-repo/semantics/openAccess
dc.title The role of (auto)-phosphorylation in the complex activation mechanism of LRRK2
dc.type info:eu-repo/semantics/article


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