The biology and pathology of the familial Parkinson's disease protein LRRK2.
Identifieur interne : 001927 ( PubMed/Corpus ); précédent : 001926; suivant : 001928The biology and pathology of the familial Parkinson's disease protein LRRK2.
Auteurs : William Dauer ; Cherry Cheng-Ying HoSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2010.
English descriptors
- KwdEn :
- MESH :
- chemical : Protein-Serine-Threonine Kinases.
- genetics : Genetic Predisposition to Disease, Mutation, Parkinson Disease.
- metabolism : Parkinson Disease.
- pathology : Parkinson Disease.
- Animals, Humans.
Abstract
Parkinson's disease (PD) is typically a sporadic illness, but the past decade has witnessed the identification of mutations responsible for multiple familial forms of the disease. The proposed functions of some of these genes (e.g., E3 ubiquitin ligase, redox-dependent chaperone) have led to the hypothesis that dysfunction of protein quality control pathways contributes to PD neurodegeneration. However, the key signaling events that act downstream of misfolded proteins to cause cell death remain poorly defined. The discovery of the familial PD kinase leucine-rich repeat kinase 2 (LRRK2) holds great promise for the elucidation of signaling events relevant to PD neurodegeneration. This review will summarize current knowledge of the clinical and cell biological features of LRRK2, the most common inherited cause of Parkinsonism.
DOI: 10.1002/mds.22717
PubMed: 20187256
Links to Exploration step
pubmed:20187256Le document en format XML
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<author><name sortKey="Ho, Cherry Cheng Ying" sort="Ho, Cherry Cheng Ying" uniqKey="Ho C" first="Cherry Cheng-Ying" last="Ho">Cherry Cheng-Ying Ho</name>
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<term>Parkinson Disease (genetics)</term>
<term>Parkinson Disease (metabolism)</term>
<term>Parkinson Disease (pathology)</term>
<term>Protein-Serine-Threonine Kinases</term>
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<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is typically a sporadic illness, but the past decade has witnessed the identification of mutations responsible for multiple familial forms of the disease. The proposed functions of some of these genes (e.g., E3 ubiquitin ligase, redox-dependent chaperone) have led to the hypothesis that dysfunction of protein quality control pathways contributes to PD neurodegeneration. However, the key signaling events that act downstream of misfolded proteins to cause cell death remain poorly defined. The discovery of the familial PD kinase leucine-rich repeat kinase 2 (LRRK2) holds great promise for the elucidation of signaling events relevant to PD neurodegeneration. This review will summarize current knowledge of the clinical and cell biological features of LRRK2, the most common inherited cause of Parkinsonism.</div>
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<Title>Movement disorders : official journal of the Movement Disorder Society</Title>
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<Abstract><AbstractText>Parkinson's disease (PD) is typically a sporadic illness, but the past decade has witnessed the identification of mutations responsible for multiple familial forms of the disease. The proposed functions of some of these genes (e.g., E3 ubiquitin ligase, redox-dependent chaperone) have led to the hypothesis that dysfunction of protein quality control pathways contributes to PD neurodegeneration. However, the key signaling events that act downstream of misfolded proteins to cause cell death remain poorly defined. The discovery of the familial PD kinase leucine-rich repeat kinase 2 (LRRK2) holds great promise for the elucidation of signaling events relevant to PD neurodegeneration. This review will summarize current knowledge of the clinical and cell biological features of LRRK2, the most common inherited cause of Parkinsonism.</AbstractText>
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