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The role of parkin in familial and sporadic Parkinson's disease

Identifieur interne : 001A62 ( Main/Corpus ); précédent : 001A61; suivant : 001A63

The role of parkin in familial and sporadic Parkinson's disease

Auteurs : Ted M. Dawson ; Valina L. Dawson

Source :

RBID : ISTEX:574280DDE25B1A05218AFEE387A41ECAF43B80AD

English descriptors

Abstract

Mutations in parkin are the second most common known cause of Parkinson's disease (PD). Parkin is an ubiquitin E3 ligase that monoubiquitinates and polyubiquitinates proteins to regulate a variety of cellular processes. Loss of parkin's E3 ligase activity is thought to play a pathogenic role in both inherited and sporadic PD. Here, we review parkin biology and pathobiology and its role in the pathogenesis of PD. © 2010 Movement Disorder Society

Url:
DOI: 10.1002/mds.22798

Links to Exploration step

ISTEX:574280DDE25B1A05218AFEE387A41ECAF43B80AD

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<affiliation>Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA</affiliation>
<affiliation>Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA</affiliation>
<affiliation>Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA</affiliation>
<description>Correspondence: Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, 733 North Broadway, BRB 731, Baltimore, MD 21205</description>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Valina L.</namePart>
<namePart type="family">Dawson</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA</affiliation>
<affiliation>Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA</affiliation>
<affiliation>Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA</affiliation>
<affiliation>Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
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<genre type="article" displayLabel="article"></genre>
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<publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<place>
<placeTerm type="text">Hoboken</placeTerm>
</place>
<dateIssued encoding="w3cdtf">2010</dateIssued>
<dateCaptured encoding="w3cdtf">2009-06-08</dateCaptured>
<dateValid encoding="w3cdtf">2009-08-21</dateValid>
<copyrightDate encoding="w3cdtf">2010</copyrightDate>
</originInfo>
<language>
<languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
</language>
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<internetMediaType>text/html</internetMediaType>
<extent unit="figures">2</extent>
<extent unit="tables">1</extent>
<extent unit="references">84</extent>
<extent unit="words">5165</extent>
</physicalDescription>
<abstract lang="en">Mutations in parkin are the second most common known cause of Parkinson's disease (PD). Parkin is an ubiquitin E3 ligase that monoubiquitinates and polyubiquitinates proteins to regulate a variety of cellular processes. Loss of parkin's E3 ligase activity is thought to play a pathogenic role in both inherited and sporadic PD. Here, we review parkin biology and pathobiology and its role in the pathogenesis of PD. © 2010 Movement Disorder Society</abstract>
<note type="content">*Potential conflict of interest: Nothing to report.</note>
<note type="funding">NIH/NINDS - No. P50 NS38377; </note>
<subject lang="en">
<genre>Keywords</genre>
<topic>ubiquitin</topic>
<topic>proteasome</topic>
<topic>PINK1</topic>
<topic>mitochondria</topic>
<topic>AIMP2</topic>
<topic>FBP‐1</topic>
</subject>
<relatedItem type="host">
<titleInfo>
<title>Movement Disorders</title>
</titleInfo>
<titleInfo type="abbreviated">
<title>Mov. Disord.</title>
</titleInfo>
<name type="personal">
<namePart type="given">Fahn</namePart>
<namePart type="family">Stanley</namePart>
<namePart type="termsOfAddress">MD</namePart>
</name>
<name type="personal">
<namePart type="given">Marder</namePart>
<namePart type="family">Karen</namePart>
<namePart type="termsOfAddress">MD</namePart>
</name>
<name type="personal">
<namePart type="given">Côté</namePart>
<namePart type="family">Lucien</namePart>
<namePart type="termsOfAddress">MD</namePart>
</name>
<name type="personal">
<namePart type="given">Reich</namePart>
<namePart type="family">Stephen G.</namePart>
<namePart type="termsOfAddress">MD</namePart>
</name>
<genre type="Journal">journal</genre>
<subject>
<genre>article category</genre>
<topic>Pathogenesis and Implications for Neuroprotection</topic>
</subject>
<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part>
<date>2010</date>
<detail type="title">
<title>Frontiers of Science and Clinical Advances in Quality of Life in Parkinson's Disease</title>
</detail>
<detail type="volume">
<caption>vol.</caption>
<number>25</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>S1</number>
</detail>
<extent unit="pages">
<start>S32</start>
<end>S39</end>
<total>8</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">574280DDE25B1A05218AFEE387A41ECAF43B80AD</identifier>
<identifier type="DOI">10.1002/mds.22798</identifier>
<identifier type="ArticleID">MDS22798</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition>
<recordInfo>
<recordContentSource>WILEY</recordContentSource>
<recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
</recordInfo>
</mods>
</metadata>
<serie></serie>
</istex>
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