Abstract
The mutations in the LRRK2 gene cause clinically typical, late-onset Parkinson disease, strengthening the idea that the familial forms of the disease represent an important tool for the study of the idiopathic forms. Despite the great effort to describe and functionally characterize the LRRK2 gene product, its physiological role remains elusive. In this article, we will discuss along with other references, our recent findings that assigned a critical role of LRR K2 protein on cytosleketal dynamics and how this direction could provide a valuable platform to further appreciate the mechanism underlying LRR K2-mediated pathophysiology of the disease.
Original language | English (US) |
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Pages (from-to) | 396-400 |
Number of pages | 5 |
Journal | Communicative and Integrative Biology |
Volume | 3 |
Issue number | 5 |
DOIs | |
State | Published - Sep 2010 |
Externally published | Yes |
Keywords
- ERM
- Filamentous actin
- G2019S
- Golgi apparatus
- LRRK2
- Microtubule
- Neuronal morphogenesis
- Parkinson disease
- Phosphorylation
- Tubulin
ASJC Scopus subject areas
- Agricultural and Biological Sciences(all)