Systematic genetic analysis of the PITX3 gene in patients with Parkinson disease
Identifieur interne : 000165 ( Istex/Corpus ); précédent : 000164; suivant : 000166Systematic genetic analysis of the PITX3 gene in patients with Parkinson disease
Auteurs : Yi Guo ; Wei-Dong Le ; Joseph Jankovic ; Hua-Rong Yang ; Hong-Bo Xu ; Wen-Jie Xie ; Zhi Song ; Hao DengSource :
- Movement Disorders [ 0885-3185 ] ; 2011-08-01.
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Abstract
Paired‐like homodomain transcription factor 3 has been found to be important for the differentiation and survival of midbrain dopaminergic neurons.
To determine whether genetic variation in the coding region of the paired‐like homodomain transcription factor 3 gene plays a role in Parkinson's disease, genetic analysis was performed in 112 patients with Parkinson's disease.
We did not identify any mutations except rs2281983, but when we extended the analysis of rs2281983 and 2 intron variants (rs4919621 and rs3758549) in 336 patients with Parkinson's disease and 244 controls, we found that rs2281983 and rs4919621 appeared to confer susceptibility to Parkinson's disease, especially in early‐onset Parkinson's disease and familial Parkinson's disease. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23693
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ISTEX:5BD9FFB534DB04A6CC579625402D89203B8CD18ELe document en format XML
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affiliationRef="#af1 #af3" corresponding="yes"><personName><givenNames>Hao</givenNames><familyName>Deng</familyName><degrees>MD, PhD</degrees></personName><contactDetails><email>hdeng008@yahoo.com</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CN" type="organization"><unparsedAffiliation>Center for Experimental Medicine and Department of Neurology, the Third Xiangya Hospital, Central South University, Changsha, China</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CN" type="organization"><unparsedAffiliation>Department of Physiology, Xiangya Medical School, Central South University, Changsha, China</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson disease</keyword><keyword xml:id="kwd2">transcription factor</keyword><keyword xml:id="kwd3">paired‐like homodomain transcription factor 3</keyword><keyword xml:id="kwd4">susceptibility</keyword></keywordGroup><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23693:MDS_23693_sm_suppinfo"></mediaResource><caption>Supporting Information</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><section xml:id="abs1-1"><title type="main">Background:</title><p>Paired‐like homodomain transcription factor 3 has been found to be important for the differentiation and survival of midbrain dopaminergic neurons.</p></section><section xml:id="abs1-2"><title type="main">Methods:</title><p>To determine whether genetic variation in the coding region of the paired‐like homodomain transcription factor 3 gene plays a role in Parkinson's disease, genetic analysis was performed in 112 patients with Parkinson's disease.</p></section><section xml:id="abs1-3"><title type="main">Results:</title><p>We did not identify any mutations except rs2281983, but when we extended the analysis of rs2281983 and 2 intron variants (rs4919621 and rs3758549) in 336 patients with Parkinson's disease and 244 controls, we found that rs2281983 and rs4919621 appeared to confer susceptibility to Parkinson's disease, especially in early‐onset Parkinson's disease and familial Parkinson's disease. © 2011 Movement Disorder Society</p></section></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Relevant conflicts of interest/financial disclosures: Nothing to report.</p></note><note xml:id="fn2"><p>This work was supported by Central South University, Changsha, China, and Baylor College of Medicine, Houston, Texas.</p></note><note xml:id="fn3"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note><note xml:id="fn4"><p>Yi Guo and Wei‐Dong Le contributed equally to this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Systematic genetic analysis of the PITX3 gene in patients with Parkinson disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Brief Report</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Systematic genetic analysis of the PITX3 gene in patients with Parkinson disease</title></titleInfo><name type="personal"><namePart type="given">Yi</namePart><namePart type="family">Guo</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Center for Experimental Medicine and Department of Neurology, the Third Xiangya Hospital, Central South University, Changsha, China</affiliation><affiliation>Department of Physiology, Xiangya Medical School, Central South University, Changsha, China</affiliation><description>Yi Guo and Wei‐Dong Le contributed equally to this article.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wei‐Dong</namePart><namePart type="family">Le</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation><description>Yi Guo and Wei‐Dong Le contributed equally to this article.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joseph</namePart><namePart type="family">Jankovic</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hua‐Rong</namePart><namePart type="family">Yang</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Center for Experimental Medicine and Department of Neurology, the Third Xiangya Hospital, Central South University, Changsha, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hong‐Bo</namePart><namePart type="family">Xu</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Center for Experimental Medicine and Department of Neurology, the Third Xiangya Hospital, Central South University, Changsha, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wen‐Jie</namePart><namePart type="family">Xie</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Zhi</namePart><namePart type="family">Song</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Center for Experimental Medicine and Department of Neurology, the Third Xiangya Hospital, Central South University, Changsha, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hao</namePart><namePart type="family">Deng</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Center for Experimental Medicine and Department of Neurology, the Third Xiangya Hospital, Central South University, Changsha, China</affiliation><affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation><affiliation>Professor of Center for Experimental Medicine and Professor of Neurology, Vice Director of Center for Experimental Medicine, the Third Xiangya Hospital, Central South University, 138 Tongzipo Road, Changsha, Hunan 410013, China</affiliation><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">2011-08-01</dateIssued><dateCaptured encoding="w3cdtf">2010-06-20</dateCaptured><dateValid encoding="w3cdtf">2011-02-01</dateValid><copyrightDate encoding="w3cdtf">2011</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="tables">2</extent><extent unit="references">20</extent><extent unit="words">3465</extent></physicalDescription><abstract>Paired‐like homodomain transcription factor 3 has been found to be important for the differentiation and survival of midbrain dopaminergic neurons.</abstract><abstract>To determine whether genetic variation in the coding region of the paired‐like homodomain transcription factor 3 gene plays a role in Parkinson's disease, genetic analysis was performed in 112 patients with Parkinson's disease.</abstract><abstract>We did not identify any mutations except rs2281983, but when we extended the analysis of rs2281983 and 2 intron variants (rs4919621 and rs3758549) in 336 patients with Parkinson's disease and 244 controls, we found that rs2281983 and rs4919621 appeared to confer susceptibility to Parkinson's disease, especially in early‐onset Parkinson's disease and familial Parkinson's disease. © 2011 Movement Disorder Society</abstract><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*This work was supported by Central South University, Changsha, China, and Baylor College of Medicine, Houston, Texas.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>keywords</genre><topic>Parkinson disease</topic><topic>transcription factor</topic><topic>paired‐like homodomain transcription factor 3</topic><topic>susceptibility</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="journal">journal</genre><note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supporting Information - </note><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>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>1729</start><end>1732</end><total>4</total></extent></part></relatedItem><identifier type="istex">5BD9FFB534DB04A6CC579625402D89203B8CD18E</identifier><identifier type="DOI">10.1002/mds.23693</identifier><identifier type="ArticleID">MDS23693</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 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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