Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women
Identifieur interne : 001B29 ( Main/Corpus ); précédent : 001B28; suivant : 001B30Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women
Auteurs : Charles E. Glatt ; Angelika D. Wahner ; Daniel J. White ; Andres Ruiz-Linares ; Beate RitzSource :
- Human Molecular Genetics [ 0964-6906 ] ; 2006-01-15.
Abstract
The vesicular monoamine transporter can protect against toxins that induce an acute parkinsonian syndrome. It has been hypothesized that cytoplasmic dopamine has subacute toxic effects in Parkinson Disease (PD) leading to neuronal death and clinical symptoms. Regulatory polymorphisms in the brain form of the vesicular monoamine transporter (VMAT2) which affect its quantitative expression might therefore serve as genetic risk factors for PD. We have screened the promoter region of the gene for VMAT2 (SLC18A2) and identified several novel polymorphisms that form discrete haplotypes. We have tested the common halpotypes in SLC18A2 for functional effects in reporter gene assays and found that there are several gain-of-function haplotypes that display significantly increased transcriptional activity from the reference element. These gain-of-function haplotypes were tested for association with PD and found to confer a protective effect that was selective for females. This finding is consistent with the prediction that increased sequestration of dopamine in secretory vesicles by VMAT2 is protective for PD.
Url:
DOI: 10.1093/hmg/ddi445
Links to Exploration step
ISTEX:5E7FE2E890C8951FF68E507D361AA487E6142A2CLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women</title><author><name sortKey="Glatt, Charles E" sort="Glatt, Charles E" uniqKey="Glatt C" first="Charles E." last="Glatt">Charles E. Glatt</name><affiliation><mods:affiliation>Department of Psychiatry, Weill Medical College of Cornell University, New York, NY 10028, USA,</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: ceg2004@med.cornell.edu</mods:affiliation></affiliation></author><author><name sortKey="Wahner, Angelika D" sort="Wahner, Angelika D" uniqKey="Wahner A" first="Angelika D." last="Wahner">Angelika D. Wahner</name><affiliation><mods:affiliation>Department of Epidemiology, School of Public Health, University of California, Los Angeles, CA 90095, USA and</mods:affiliation></affiliation></author><author><name sortKey="White, Daniel J" sort="White, Daniel J" uniqKey="White D" first="Daniel J." last="White">Daniel J. White</name><affiliation><mods:affiliation>The Galton Laboratory, University College London, UK</mods:affiliation></affiliation></author><author><name sortKey="Ruiz Linares, Andres" sort="Ruiz Linares, Andres" uniqKey="Ruiz Linares A" first="Andres" last="Ruiz-Linares">Andres Ruiz-Linares</name><affiliation><mods:affiliation>The Galton Laboratory, University College London, UK</mods:affiliation></affiliation></author><author><name sortKey="Ritz, Beate" sort="Ritz, Beate" uniqKey="Ritz B" first="Beate" last="Ritz">Beate Ritz</name><affiliation><mods:affiliation>Department of Epidemiology, School of Public Health, University of California, Los Angeles, CA 90095, USA and</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:5E7FE2E890C8951FF68E507D361AA487E6142A2C</idno><date when="2006" year="2006">2006</date><idno type="doi">10.1093/hmg/ddi445</idno><idno type="url">https://api.istex.fr/document/5E7FE2E890C8951FF68E507D361AA487E6142A2C/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001B29</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women</title><author><name sortKey="Glatt, Charles E" sort="Glatt, Charles E" uniqKey="Glatt C" first="Charles E." last="Glatt">Charles E. Glatt</name><affiliation><mods:affiliation>Department of Psychiatry, Weill Medical College of Cornell University, New York, NY 10028, USA,</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: ceg2004@med.cornell.edu</mods:affiliation></affiliation></author><author><name sortKey="Wahner, Angelika D" sort="Wahner, Angelika D" uniqKey="Wahner A" first="Angelika D." last="Wahner">Angelika D. Wahner</name><affiliation><mods:affiliation>Department of Epidemiology, School of Public Health, University of California, Los Angeles, CA 90095, USA and</mods:affiliation></affiliation></author><author><name sortKey="White, Daniel J" sort="White, Daniel J" uniqKey="White D" first="Daniel J." last="White">Daniel J. White</name><affiliation><mods:affiliation>The Galton Laboratory, University College London, UK</mods:affiliation></affiliation></author><author><name sortKey="Ruiz Linares, Andres" sort="Ruiz Linares, Andres" uniqKey="Ruiz Linares A" first="Andres" last="Ruiz-Linares">Andres Ruiz-Linares</name><affiliation><mods:affiliation>The Galton Laboratory, University College London, UK</mods:affiliation></affiliation></author><author><name sortKey="Ritz, Beate" sort="Ritz, Beate" uniqKey="Ritz B" first="Beate" last="Ritz">Beate Ritz</name><affiliation><mods:affiliation>Department of Epidemiology, School of Public Health, University of California, Los Angeles, CA 90095, USA and</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Human Molecular Genetics</title><title level="j" type="abbrev">Hum. Mol. Genet.</title><idno type="ISSN">0964-6906</idno><idno type="eISSN">1460-2083</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2006-01-15">2006-01-15</date><biblScope unit="volume">15</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="299">299</biblScope><biblScope unit="page" to="305">305</biblScope></imprint><idno type="ISSN">0964-6906</idno></series><idno type="istex">5E7FE2E890C8951FF68E507D361AA487E6142A2C</idno><idno type="DOI">10.1093/hmg/ddi445</idno><idno type="href">ddi445</idno><idno type="local">ddi445</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0964-6906</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The vesicular monoamine transporter can protect against toxins that induce an acute parkinsonian syndrome. It has been hypothesized that cytoplasmic dopamine has subacute toxic effects in Parkinson Disease (PD) leading to neuronal death and clinical symptoms. Regulatory polymorphisms in the brain form of the vesicular monoamine transporter (VMAT2) which affect its quantitative expression might therefore serve as genetic risk factors for PD. We have screened the promoter region of the gene for VMAT2 (SLC18A2) and identified several novel polymorphisms that form discrete haplotypes. We have tested the common halpotypes in SLC18A2 for functional effects in reporter gene assays and found that there are several gain-of-function haplotypes that display significantly increased transcriptional activity from the reference element. These gain-of-function haplotypes were tested for association with PD and found to confer a protective effect that was selective for females. This finding is consistent with the prediction that increased sequestration of dopamine in secretory vesicles by VMAT2 is protective for PD.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Charles E. Glatt</name><affiliations><json:string>Department of Psychiatry, Weill Medical College of Cornell University, New York, NY 10028, USA,</json:string><json:string>E-mail: ceg2004@med.cornell.edu</json:string></affiliations></json:item><json:item><name>Angelika D. Wahner</name><affiliations><json:string>Department of Epidemiology, School of Public Health, University of California, Los Angeles, CA 90095, USA and</json:string></affiliations></json:item><json:item><name>Daniel J. White</name><affiliations><json:string>The Galton Laboratory, University College London, UK</json:string></affiliations></json:item><json:item><name>Andres Ruiz-Linares</name><affiliations><json:string>The Galton Laboratory, University College London, UK</json:string></affiliations></json:item><json:item><name>Beate Ritz</name><affiliations><json:string>Department of Epidemiology, School of Public Health, University of California, Los Angeles, CA 90095, USA and</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>ARTICLES</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The vesicular monoamine transporter can protect against toxins that induce an acute parkinsonian syndrome. It has been hypothesized that cytoplasmic dopamine has subacute toxic effects in Parkinson Disease (PD) leading to neuronal death and clinical symptoms. Regulatory polymorphisms in the brain form of the vesicular monoamine transporter (VMAT2) which affect its quantitative expression might therefore serve as genetic risk factors for PD. We have screened the promoter region of the gene for VMAT2 (SLC18A2) and identified several novel polymorphisms that form discrete haplotypes. We have tested the common halpotypes in SLC18A2 for functional effects in reporter gene assays and found that there are several gain-of-function haplotypes that display significantly increased transcriptional activity from the reference element. These gain-of-function haplotypes were tested for association with PD and found to confer a protective effect that was selective for females. This finding is consistent with the prediction that increased sequestration of dopamine in secretory vesicles by VMAT2 is protective for PD.</abstract><qualityIndicators><score>6.896</score><pdfVersion>1.2</pdfVersion><pdfPageSize>610 x 795 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>1</keywordCount><abstractCharCount>1116</abstractCharCount><pdfWordCount>5047</pdfWordCount><pdfCharCount>33328</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>158</abstractWordCount></qualityIndicators><title>Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women</title><genre><json:string>research-article</json:string></genre><host><volume>15</volume><pages><last>305</last><first>299</first></pages><issn><json:string>0964-6906</json:string></issn><issue>2</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-2083</json:string></eissn><title>Human Molecular Genetics</title></host><categories><wos><json:string>BIOCHEMISTRY & MOLECULAR BIOLOGY</json:string><json:string>GENETICS & HEREDITY</json:string></wos></categories><publicationDate>2006</publicationDate><copyrightDate>2006</copyrightDate><doi><json:string>10.1093/hmg/ddi445</json:string></doi><id>5E7FE2E890C8951FF68E507D361AA487E6142A2C</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/5E7FE2E890C8951FF68E507D361AA487E6142A2C/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/5E7FE2E890C8951FF68E507D361AA487E6142A2C/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/5E7FE2E890C8951FF68E507D361AA487E6142A2C/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women</title><respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>OUP</p></availability><date>2005-12-08</date></publicationStmt><notesStmt><note>*To whom correspondence should be addressed at: Department of Psychiatry, Weill Medical College of Cornell University, Room LC907A, Box 244, 1300 York Avenue, New York, NY 10021, USA. Tel: +1 2127466723; Fax: +1 2127468529; Email: ceg2004@med.cornell.edu</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women</title><author><persName><forename type="first">Charles E.</forename><surname>Glatt</surname></persName><email>ceg2004@med.cornell.edu</email><affiliation>Department of Psychiatry, Weill Medical College of Cornell University, New York, NY 10028, USA,</affiliation></author><author><persName><forename type="first">Angelika D.</forename><surname>Wahner</surname></persName><affiliation>Department of Epidemiology, School of Public Health, University of California, Los Angeles, CA 90095, USA and</affiliation></author><author><persName><forename type="first">Daniel J.</forename><surname>White</surname></persName><affiliation>The Galton Laboratory, University College London, UK</affiliation></author><author><persName><forename type="first">Andres</forename><surname>Ruiz-Linares</surname></persName><affiliation>The Galton Laboratory, University College London, UK</affiliation></author><author><persName><forename type="first">Beate</forename><surname>Ritz</surname></persName><affiliation>Department of Epidemiology, School of Public Health, University of California, Los Angeles, CA 90095, USA and</affiliation></author></analytic><monogr><title level="j">Human Molecular Genetics</title><title level="j" type="abbrev">Hum. Mol. Genet.</title><idno type="pISSN">0964-6906</idno><idno type="eISSN">1460-2083</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2006-01-15"></date><biblScope unit="volume">15</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="299">299</biblScope><biblScope unit="page" to="305">305</biblScope></imprint></monogr><idno type="istex">5E7FE2E890C8951FF68E507D361AA487E6142A2C</idno><idno type="DOI">10.1093/hmg/ddi445</idno><idno type="href">ddi445</idno><idno type="local">ddi445</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005-12-08</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The vesicular monoamine transporter can protect against toxins that induce an acute parkinsonian syndrome. It has been hypothesized that cytoplasmic dopamine has subacute toxic effects in Parkinson Disease (PD) leading to neuronal death and clinical symptoms. Regulatory polymorphisms in the brain form of the vesicular monoamine transporter (VMAT2) which affect its quantitative expression might therefore serve as genetic risk factors for PD. We have screened the promoter region of the gene for VMAT2 (SLC18A2) and identified several novel polymorphisms that form discrete haplotypes. We have tested the common halpotypes in SLC18A2 for functional effects in reporter gene assays and found that there are several gain-of-function haplotypes that display significantly increased transcriptional activity from the reference element. These gain-of-function haplotypes were tested for association with PD and found to confer a protective effect that was selective for females. This finding is consistent with the prediction that increased sequestration of dopamine in secretory vesicles by VMAT2 is protective for PD.</p></abstract></profileDesc><revisionDesc><change when="2005-12-08">Created</change><change when="2006-01-15">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-15">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/5E7FE2E890C8951FF68E507D361AA487E6142A2C/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="US-ASCII"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article xml:lang="en" article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">hmg</journal-id><journal-id journal-id-type="nlm-ta">Hum Mol Genet</journal-id><journal-id journal-id-type="publisher-id">hmg</journal-id><journal-title>Human Molecular Genetics</journal-title><abbrev-journal-title abbrev-type="publisher">Hum. Mol. Genet.</abbrev-journal-title><issn pub-type="ppub">0964-6906</issn><issn pub-type="epub">1460-2083</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="other">ddi445</article-id><article-id pub-id-type="doi">10.1093/hmg/ddi445</article-id><article-categories><subj-group subj-group-type="heading"><subject>ARTICLES</subject></subj-group></article-categories><title-group><article-title>Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Glatt</surname><given-names>Charles E.</given-names></name><xref rid="AF1">1</xref><xref rid="COR1">*</xref></contrib><contrib contrib-type="author"><name><surname>Wahner</surname><given-names>Angelika D.</given-names></name><xref rid="AF2">2</xref></contrib><contrib contrib-type="author"><name><surname>White</surname><given-names>Daniel J.</given-names></name><xref rid="AF3">3</xref></contrib><contrib contrib-type="author"><name><surname>Ruiz-Linares</surname><given-names>Andres</given-names></name><xref rid="AF3">3</xref></contrib><contrib contrib-type="author"><name><surname>Ritz</surname><given-names>Beate</given-names></name><xref rid="AF2">2</xref></contrib><aff id="AF1"><sup>1</sup>Department of Psychiatry, Weill Medical College of Cornell University, New York, NY 10028, USA,</aff><aff id="AF2"><sup>2</sup>Department of Epidemiology, School of Public Health, University of California, Los Angeles, CA 90095, USA and</aff><aff id="AF3"><sup>3</sup>The Galton Laboratory, University College London, UK</aff></contrib-group><author-notes><corresp id="COR1"><label>*</label>To whom correspondence should be addressed at: Department of Psychiatry, Weill Medical College of Cornell University, Room LC907A, Box 244, 1300 York Avenue, New York, NY 10021, USA. Tel: +1 2127466723; Fax: +1 2127468529; Email: <ext-link xlink:href="ceg2004@med.cornell.edu" ext-link-type="email">ceg2004@med.cornell.edu</ext-link></corresp></author-notes><pub-date pub-type="epub"><day>8</day><month>12</month><year>2005</year></pub-date><pub-date pub-type="ppub"><day>15</day><month>January</month><year>2006</year></pub-date><volume>15</volume><issue>2</issue><fpage>299</fpage><lpage>305</lpage><history><date date-type="accepted"><day>28</day><month>11</month><year>2005</year></date><date date-type="received"><day>21</day><month>10</month><year>2005</year></date></history><permissions><copyright-statement>© The Author 2005. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</copyright-statement><copyright-year>2006</copyright-year></permissions><self-uri content-type="arthw-pdf" xlink:href="ddi445"></self-uri><abstract xml:lang="en"><p>The vesicular monoamine transporter can protect against toxins that induce an acute parkinsonian syndrome. It has been hypothesized that cytoplasmic dopamine has subacute toxic effects in Parkinson Disease (PD) leading to neuronal death and clinical symptoms. Regulatory polymorphisms in the brain form of the vesicular monoamine transporter (VMAT2) which affect its quantitative expression might therefore serve as genetic risk factors for PD. We have screened the promoter region of the gene for VMAT2 (SLC18A2) and identified several novel polymorphisms that form discrete haplotypes. We have tested the common halpotypes in SLC18A2 for functional effects in reporter gene assays and found that there are several gain-of-function haplotypes that display significantly increased transcriptional activity from the reference element. These gain-of-function haplotypes were tested for association with PD and found to confer a protective effect that was selective for females. This finding is consistent with the prediction that increased sequestration of dopamine in secretory vesicles by VMAT2 is protective for PD.</p></abstract><custom-meta-wrap><custom-meta><meta-name>hwp-legacy-fpage</meta-name><meta-value>299</meta-value></custom-meta><custom-meta><meta-name>cover-date</meta-name><meta-value>15 January 2006</meta-value></custom-meta><custom-meta><meta-name>hwp-legacy-dochead</meta-name><meta-value>Article</meta-value></custom-meta></custom-meta-wrap></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women</title></titleInfo><name type="personal"><namePart type="given">Charles E.</namePart><namePart type="family">Glatt</namePart><affiliation>Department of Psychiatry, Weill Medical College of Cornell University, New York, NY 10028, USA,</affiliation><affiliation>E-mail: ceg2004@med.cornell.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Angelika D.</namePart><namePart type="family">Wahner</namePart><affiliation>Department of Epidemiology, School of Public Health, University of California, Los Angeles, CA 90095, USA and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daniel J.</namePart><namePart type="family">White</namePart><affiliation>The Galton Laboratory, University College London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andres</namePart><namePart type="family">Ruiz-Linares</namePart><affiliation>The Galton Laboratory, University College London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Beate</namePart><namePart type="family">Ritz</namePart><affiliation>Department of Epidemiology, School of Public Health, University of California, Los Angeles, CA 90095, USA and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2006-01-15</dateIssued><dateCreated encoding="w3cdtf">2005-12-08</dateCreated><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">The vesicular monoamine transporter can protect against toxins that induce an acute parkinsonian syndrome. It has been hypothesized that cytoplasmic dopamine has subacute toxic effects in Parkinson Disease (PD) leading to neuronal death and clinical symptoms. Regulatory polymorphisms in the brain form of the vesicular monoamine transporter (VMAT2) which affect its quantitative expression might therefore serve as genetic risk factors for PD. We have screened the promoter region of the gene for VMAT2 (SLC18A2) and identified several novel polymorphisms that form discrete haplotypes. We have tested the common halpotypes in SLC18A2 for functional effects in reporter gene assays and found that there are several gain-of-function haplotypes that display significantly increased transcriptional activity from the reference element. These gain-of-function haplotypes were tested for association with PD and found to confer a protective effect that was selective for females. This finding is consistent with the prediction that increased sequestration of dopamine in secretory vesicles by VMAT2 is protective for PD.</abstract><note type="author-notes">*To whom correspondence should be addressed at: Department of Psychiatry, Weill Medical College of Cornell University, Room LC907A, Box 244, 1300 York Avenue, New York, NY 10021, USA. Tel: +1 2127466723; Fax: +1 2127468529; Email: ceg2004@med.cornell.edu</note><relatedItem type="host"><titleInfo><title>Human Molecular Genetics</title></titleInfo><titleInfo type="abbreviated"><title>Hum. Mol. Genet.</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0964-6906</identifier><identifier type="eISSN">1460-2083</identifier><identifier type="PublisherID">hmg</identifier><identifier type="PublisherID-hwp">hmg</identifier><identifier type="PublisherID-nlm-ta">Hum Mol Genet</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>15</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>299</start><end>305</end></extent></part></relatedItem><identifier type="istex">5E7FE2E890C8951FF68E507D361AA487E6142A2C</identifier><identifier type="DOI">10.1093/hmg/ddi445</identifier><identifier type="href">ddi445</identifier><identifier type="local">ddi445</identifier><accessCondition type="use and reproduction" contentType="copyright">© The Author 2005. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><covers><json:item><original>true</original><mimetype>image/tiff</mimetype><extension>tiff</extension><uri>https://api.istex.fr/document/5E7FE2E890C8951FF68E507D361AA487E6142A2C/covers/tiff</uri></json:item><json:item><original>true</original><mimetype>text/html</mimetype><extension>html</extension><uri>https://api.istex.fr/document/5E7FE2E890C8951FF68E507D361AA487E6142A2C/covers/html</uri></json:item></covers><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/5E7FE2E890C8951FF68E507D361AA487E6142A2C/annexes/jpeg</uri></json:item><json:item><original>true</original><mimetype>image/gif</mimetype><extension>gif</extension><uri>https://api.istex.fr/document/5E7FE2E890C8951FF68E507D361AA487E6142A2C/annexes/gif</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/5E7FE2E890C8951FF68E507D361AA487E6142A2C/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">BIOCHEMISTRY & MOLECULAR BIOLOGY</classCode><classCode scheme="WOS">GENETICS & HEREDITY</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001B29 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 001B29 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:5E7FE2E890C8951FF68E507D361AA487E6142A2C
|texte= Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women
}}
| This area was generated with Dilib version V0.6.23. |  |