The biology and pathology of the familial Parkinson's disease protein LRRK2
Identifieur interne : 000523 ( Main/Exploration ); précédent : 000522; suivant : 000524The biology and pathology of the familial Parkinson's disease protein LRRK2
Auteurs : William Dauer [États-Unis] ; Cherry Cheng-Ying Ho [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2010.
English descriptors
- KwdEn :
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. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.22717
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">The biology and pathology of the familial Parkinson's disease protein LRRK2</title><author><name sortKey="Dauer, William" sort="Dauer, William" uniqKey="Dauer W" first="William" last="Dauer">William Dauer</name></author><author><name sortKey="Ho, Cherry Cheng Ing" sort="Ho, Cherry Cheng Ing" uniqKey="Ho C" first="Cherry Cheng-Ying" last="Ho">Cherry Cheng-Ying Ho</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:758F518B9D51EBDB4D02C2B1F2F86C5C4AA67683</idno><date when="2010" year="2010">2010</date><idno type="doi">10.1002/mds.22717</idno><idno type="url">https://api.istex.fr/document/758F518B9D51EBDB4D02C2B1F2F86C5C4AA67683/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001227</idno><idno type="wicri:Area/Main/Curation">001026</idno><idno type="wicri:Area/Main/Exploration">000523</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">The biology and pathology of the familial Parkinson's disease protein LRRK2</title><author><name sortKey="Dauer, William" sort="Dauer, William" uniqKey="Dauer W" first="William" last="Dauer">William Dauer</name><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region><settlement type="city">New York</settlement></placeName><orgName type="university">Université Columbia</orgName></affiliation><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pharmacology, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region><settlement type="city">New York</settlement></placeName><orgName type="university">Université Columbia</orgName></affiliation></author><author><name sortKey="Ho, Cherry Cheng Ing" sort="Ho, Cherry Cheng Ing" uniqKey="Ho C" first="Cherry Cheng-Ying" last="Ho">Cherry Cheng-Ying Ho</name><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Columbia University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region><settlement type="city">New York</settlement></placeName><orgName type="university">Université Columbia</orgName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010">2010</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">S1</biblScope><biblScope unit="page" from="S40">S40</biblScope><biblScope unit="page" to="S43">S43</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">758F518B9D51EBDB4D02C2B1F2F86C5C4AA67683</idno><idno type="DOI">10.1002/mds.22717</idno><idno type="ArticleID">MDS22717</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>LRRK2</term><term>Parkinson's disease</term><term>neurodegeneration</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><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. © 2010 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region><settlement><li>New York</li></settlement><orgName><li>Université Columbia</li></orgName></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Dauer, William" sort="Dauer, William" uniqKey="Dauer W" first="William" last="Dauer">William Dauer</name></region><name sortKey="Dauer, William" sort="Dauer, William" uniqKey="Dauer W" first="William" last="Dauer">William Dauer</name><name sortKey="Ho, Cherry Cheng Ing" sort="Ho, Cherry Cheng Ing" uniqKey="Ho C" first="Cherry Cheng-Ying" last="Ho">Cherry Cheng-Ying Ho</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000523 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000523 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= ISTEX:758F518B9D51EBDB4D02C2B1F2F86C5C4AA67683
|texte= The biology and pathology of the familial Parkinson's disease protein LRRK2
}}
| This area was generated with Dilib version V0.6.23. |  |