Journal
PARKINSONISM & RELATED DISORDERS
Volume 13, Issue 7, Pages 382-385Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.parkreldis.2007.01.008
Keywords
Lrrk2; interactors; tandem mass spectrometry
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Funding
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P01NS040256, P50NS040256] Funding Source: NIH RePORTER
- NINDS NIH HHS [P01 NS040256, P50 NS040256, P50 NS040256-080004, P50 NS40256] Funding Source: Medline
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Pathogenic substitutions in the Lrrk2 protein have been shown to be an important cause of both familial and sporadic parkinsonism. The molecular pathway involved in Lrrk2 dopaminergic neuron degeneration remains elusive. Employing a combination of Lrrk2-mediated protein precipitation and tandem mass spectrometry, we identified 14 potential Lrrk2 binding partners. The majority of these interactions may be subgrouped into three functional cellular pathways: (i) chaperone-mediated response, (ii) proteins associated with the cytoskeleton and trafficking and (iii) phosphorylation and kinase activity. Future investigation of these candidates is now warranted and may help resolve the pathomechanism behind Lrrk2 neurodegeneration. (C) 2007 Elsevier Ltd. All rights reserved.
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