LRRK2 in Parkinson's disease: function in cells and neurodegeneration.
LRRK2 in Parkinson's disease: function in cells and neurodegeneration.
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DOI：
10.1111/j.1742-4658.2009.07342.x
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发表时间：
2009-11
期刊：
影响因子：
--
通讯作者：
West AB
中科院分区：
文献类型：
--
作者：
Webber PJ;West AB
Detailed characterization of LRRK2 function may provide insight into the molecular basis of neurodegeneration in Parkinson’s disease (PD) since mutations in LRRK2 cause a phenotype with strong overlap to typical late-onset disease and LRRK2 mutations are responsible for significant proportions of PD in some populations. The complexity of large multi-domain protein kinases like LRRK2 challenge traditional functional approaches, although initial studies have successfully defined the basic mechanisms of enzyme activity with putative effects of pathogenic mutations on kinase activity. The role of LRRK2 in cells remains elusive, with potential function in MAP kinase pathways, protein translation control, programmed cell death pathways, and activity in cytoskeleton dynamics. The initial focus on LRRK2-kinase dependent phenomena places emphasis on the discovery of LRRK2 kinase substrates, although candidate substrates are yet confined to in vitro assays. Herein, hypothetical mechanisms for LRRK2-mediated cell death and kinase activation are proposed. As a promising target for neuroprotection strategies in PD, in vitro and in vivo models that accurately demonstrate LRRK2 function relevant to neurodegeneration will aide in the identification of molecules with the highest chance for success in the clinic.
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