Haplotype analysis of the PARK 11 gene, GIGYF2, in sporadic Parkinson's disease
Identifieur interne : 001747 ( Main/Corpus ); précédent : 001746; suivant : 001748Haplotype analysis of the PARK 11 gene, GIGYF2, in sporadic Parkinson's disease
Auteurs : Greg T. Sutherland ; Gerhard A. Siebert ; Jeremy R. B. Newman ; Peter A. Silburn ; Richard S. Boyle ; John D. O'Sullivan ; George D. MellickSource :
- Movement Disorders [ 0885-3185 ] ; 2009-02-15.
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Abstract
Familial Parkinsonism (PARK) genes are strong candidates for conferring susceptibility to common forms of PD. However, most studies to date have provided little evidence that their common variants substantially influence disease risk. Recently, mutations were described in the gene, GIGYF2 (TNRC15), located at the PARK11 locus (2q37.1). Here, we use a haplotype tagging approach to examine common variation in the GIGYF2 gene and PD risk. PD cases (n = 568) and age and gender‐matched control subjects (n = 568) were recruited from three specialist movement disorder clinics in Brisbane (Australia) and the Australian electoral roll. Twelve tagging SNPs were assessed in all subjects and haplotype and genotype associations were explored. Overall our findings suggest that common genetic variants of GIGYF2 do not significantly affect sporadic PD risk in Australian Caucasians. © 2008 Movement Disorder Society
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DOI: 10.1002/mds.22427
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ISTEX:5C520A1A32A512B867E533B866B8964343315BB3Le document en format XML
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However, most studies to date have provided little evidence that their common variants substantially influence disease risk. Recently, mutations were described in the gene, GIGYF2 (TNRC15), located at the PARK11 locus (2q37.1). Here, we use a haplotype tagging approach to examine common variation in the GIGYF2 gene and PD risk. PD cases (n = 568) and age and gender‐matched control subjects (n = 568) were recruited from three specialist movement disorder clinics in Brisbane (Australia) and the Australian electoral roll. Twelve tagging SNPs were assessed in all subjects and haplotype and genotype associations were explored. Overall our findings suggest that common genetic variants of GIGYF2 do not significantly affect sporadic PD risk in Australian Caucasians. © 2008 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Greg T. 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However, most studies to date have provided little evidence that their common variants substantially influence disease risk. Recently, mutations were described in the gene, GIGYF2 (TNRC15), located at the PARK11 locus (2q37.1). Here, we use a haplotype tagging approach to examine common variation in the GIGYF2 gene and PD risk. PD cases (n = 568) and age and gender‐matched control subjects (n = 568) were recruited from three specialist movement disorder clinics in Brisbane (Australia) and the Australian electoral roll. Twelve tagging SNPs were assessed in all subjects and haplotype and genotype associations were explored. 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B.</givenNames><familyName>Newman</familyName><degrees>BBiomedSc</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Peter A.</givenNames><familyName>Silburn</familyName><degrees>PhD, FRACP</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Richard S.</givenNames><familyName>Boyle</familyName><degrees>FRACP</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af4"><personName><givenNames>John D.</givenNames><familyName>O'Sullivan</familyName><degrees>FRACP</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1 #af3 #af4" corresponding="yes"><personName><givenNames>George D.</givenNames><familyName>Mellick</familyName><degrees>PhD</degrees></personName><contactDetails><email>g.sutherland@griffith.edu.au</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="AU" type="organization"><unparsedAffiliation>Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Brisbane, Queensland, Australia</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="AU" type="organization"><unparsedAffiliation>UQ Centre for Clinical Research, School of Medicine, University of Queensland, Brisbane, Queensland Australia</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="AU" type="organization"><unparsedAffiliation>Department of Neurology, Princess Alexandra Hospital, Brisbane, Queensland, Australia</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="AU" type="organization"><unparsedAffiliation>Department of Neurology, Royal Brisbane and Women's Hospital, Brisbane, Queensland, Australia</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">PD‐related genes</keyword><keyword xml:id="kwd3">association</keyword></keywordGroup><fundingInfo><fundingAgency>NHMRC</fundingAgency><fundingNumber>#401537</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Geriatric Medical Foundation of Queensland (GS)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Princess Alexandra Hospital Department of Neurology</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Royal Brisbane Hospital Foundation</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Familial Parkinsonism (<i>PARK</i>) genes are strong candidates for conferring susceptibility to common forms of PD. However, most studies to date have provided little evidence that their common variants substantially influence disease risk. Recently, mutations were described in the gene, <i>GIGYF2</i> (<i>TNRC15</i>), located at the <i>PARK</i>11 locus (2q37.1). Here, we use a haplotype tagging approach to examine common variation in the <i>GIGYF2</i> gene and PD risk. PD cases (n = 568) and age and gender‐matched control subjects (n = 568) were recruited from three specialist movement disorder clinics in Brisbane (Australia) and the Australian electoral roll. Twelve tagging SNPs were assessed in all subjects and haplotype and genotype associations were explored. Overall our findings suggest that common genetic variants of <i>GIGYF2</i> do not significantly affect sporadic PD risk in Australian Caucasians. © 2008 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: None reported.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Haplotype analysis of the PARK 11 gene, GIGYF2, in sporadic Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>PARK 11 and Sporadic Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Haplotype analysis of the</title></titleInfo><name type="personal"><namePart type="given">Greg T.</namePart><namePart type="family">Sutherland</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Brisbane, Queensland, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gerhard A.</namePart><namePart type="family">Siebert</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Brisbane, Queensland, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jeremy R. B.</namePart><namePart type="family">Newman</namePart><namePart type="termsOfAddress">BBiomedSc</namePart><affiliation>Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Brisbane, Queensland, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter A.</namePart><namePart type="family">Silburn</namePart><namePart type="termsOfAddress">PhD, FRACP</namePart><affiliation>Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Brisbane, Queensland, Australia</affiliation><affiliation>UQ Centre for Clinical Research, School of Medicine, University of Queensland, Brisbane, Queensland Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Richard S.</namePart><namePart type="family">Boyle</namePart><namePart type="termsOfAddress">FRACP</namePart><affiliation>Department of Neurology, Princess Alexandra Hospital, Brisbane, Queensland, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John D.</namePart><namePart type="family">O'Sullivan</namePart><namePart type="termsOfAddress">FRACP</namePart><affiliation>Department of Neurology, Royal Brisbane and Women's Hospital, Brisbane, Queensland, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">George D.</namePart><namePart type="family">Mellick</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Brisbane, Queensland, Australia</affiliation><affiliation>Department of Neurology, Princess Alexandra Hospital, Brisbane, Queensland, Australia</affiliation><affiliation>Department of Neurology, Royal Brisbane and Women's Hospital, Brisbane, Queensland, Australia</affiliation><description>Correspondence: Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Nathan, Queensland 4111, Australia</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-02-15</dateIssued><dateCaptured encoding="w3cdtf">2008-10-07</dateCaptured><dateValid encoding="w3cdtf">2008-11-27</dateValid><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">2</extent><extent unit="references">21</extent><extent unit="words">2812</extent></physicalDescription><abstract lang="en">Familial Parkinsonism (PARK) genes are strong candidates for conferring susceptibility to common forms of PD. However, most studies to date have provided little evidence that their common variants substantially influence disease risk. Recently, mutations were described in the gene, GIGYF2 (TNRC15), located at the PARK11 locus (2q37.1). Here, we use a haplotype tagging approach to examine common variation in the GIGYF2 gene and PD risk. PD cases (n = 568) and age and gender‐matched control subjects (n = 568) were recruited from three specialist movement disorder clinics in Brisbane (Australia) and the Australian electoral roll. Twelve tagging SNPs were assessed in all subjects and haplotype and genotype associations were explored. Overall our findings suggest that common genetic variants of GIGYF2 do not significantly affect sporadic PD risk in Australian Caucasians. © 2008 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None reported.</note><note type="funding">NHMRC - No. #401537; </note><note type="funding">Geriatric Medical Foundation of Queensland (GS)</note><note type="funding">Princess Alexandra Hospital Department of Neurology</note><note type="funding">Royal Brisbane Hospital Foundation</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>PD‐related genes</topic><topic>association</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Brief Report</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>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>448</start><end>452</end><total>5</total></extent></part></relatedItem><identifier type="istex">5C520A1A32A512B867E533B866B8964343315BB3</identifier><identifier type="DOI">10.1002/mds.22427</identifier><identifier type="ArticleID">MDS22427</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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