Functional association of the parkin gene promoter with idiopathic Parkinson's disease
Identifieur interne : 003097 ( Main/Corpus ); précédent : 003096; suivant : 003098Functional association of the parkin gene promoter with idiopathic Parkinson's disease
Auteurs : Andrew B. West ; Demetrius Maraganore ; Julia Crook ; Tim Lesnick ; Paul J. Lockhart ; Kristen M. Wilkes ; Gregory Kapatos ; John A. Hardy ; Matt J. FarrerSource :
- Human Molecular Genetics [ 0964-6906 ] ; 2002-10-15.
Abstract
Loss-of-function mutations in the parkin gene were first identified in autosomal recessive juvenile parkinsonism (AR-JP). Subsequently, parkin mutations were found in many early-onset patients with Parkinson's disease (PD) (<45 years at onset). We hypothesized that parkin gene expression also may contribute to the age-associated risk of idiopathic PD (>50 years at onset). Two single-nucleotide polymorphisms within the parkin core promoter have been identified and assessed. We show one of the variants, −258 T/G, is located in a region of DNA that binds nuclear protein from human substantia nigra in vitro and functionally affects gene transcription. Furthermore, the −258 T/G polymorphism is genetically associated with idiopathic PD, as assessed in a large population-based series of cases and controls. Our results further implicate the parkin gene in the development of Parkinson's disease.
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DOI: 10.1093/hmg/11.22.2787
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West</name><affiliation><mods:affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</mods:affiliation></affiliation></author><author><name sortKey="Maraganore, Demetrius" sort="Maraganore, Demetrius" uniqKey="Maraganore D" first="Demetrius" last="Maraganore">Demetrius Maraganore</name><affiliation><mods:affiliation>Department of Neurology and</mods:affiliation></affiliation></author><author><name sortKey="Crook, Julia" sort="Crook, Julia" uniqKey="Crook J" first="Julia" last="Crook">Julia Crook</name><affiliation><mods:affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</mods:affiliation></affiliation></author><author><name sortKey="Lesnick, Tim" sort="Lesnick, Tim" uniqKey="Lesnick T" first="Tim" last="Lesnick">Tim Lesnick</name><affiliation><mods:affiliation>Division of Biostatistics, HSR, Mayo Clinic and Mayo Foundation, Rochester,MN 55905 USA and</mods:affiliation></affiliation></author><author><name sortKey="Lockhart, Paul J" sort="Lockhart, Paul J" uniqKey="Lockhart P" first="Paul J." last="Lockhart">Paul J. 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Wilkes</name><affiliation><mods:affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</mods:affiliation></affiliation></author><author><name sortKey="Kapatos, Gregory" sort="Kapatos, Gregory" uniqKey="Kapatos G" first="Gregory" last="Kapatos">Gregory Kapatos</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Neurosciences and Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA</mods:affiliation></affiliation></author><author><name sortKey="Hardy, John A" sort="Hardy, John A" uniqKey="Hardy J" first="John A." last="Hardy">John A. Hardy</name><affiliation><mods:affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</mods:affiliation></affiliation></author><author><name sortKey="Farrer, Matt J" sort="Farrer, Matt J" uniqKey="Farrer M" first="Matt J." last="Farrer">Matt J. Farrer</name></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="2002-10-15">2002-10-15</date><biblScope unit="volume">11</biblScope><biblScope unit="issue">22</biblScope><biblScope unit="page" from="2787">2787</biblScope><biblScope unit="page" to="2792">2792</biblScope></imprint><idno type="ISSN">0964-6906</idno></series><idno type="istex">93538F48DC6955C6C824E588DE9A4352133D970B</idno><idno type="DOI">10.1093/hmg/11.22.2787</idno><idno type="local">ddf259</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">Loss-of-function mutations in the parkin gene were first identified in autosomal recessive juvenile parkinsonism (AR-JP). Subsequently, parkin mutations were found in many early-onset patients with Parkinson's disease (PD) (<45 years at onset). We hypothesized that parkin gene expression also may contribute to the age-associated risk of idiopathic PD (>50 years at onset). Two single-nucleotide polymorphisms within the parkin core promoter have been identified and assessed. We show one of the variants, −258 T/G, is located in a region of DNA that binds nuclear protein from human substantia nigra in vitro and functionally affects gene transcription. Furthermore, the −258 T/G polymorphism is genetically associated with idiopathic PD, as assessed in a large population-based series of cases and controls. Our results further implicate the parkin gene in the development of Parkinson's disease.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Andrew B. West</name><affiliations><json:string>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</json:string></affiliations></json:item><json:item><name>Demetrius Maraganore</name><affiliations><json:string>Department of Neurology and</json:string></affiliations></json:item><json:item><name>Julia Crook</name><affiliations><json:string>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</json:string></affiliations></json:item><json:item><name>Tim Lesnick</name><affiliations><json:string>Division of Biostatistics, HSR, Mayo Clinic and Mayo Foundation, Rochester,MN 55905 USA and</json:string></affiliations></json:item><json:item><name>Paul J. Lockhart</name><affiliations><json:string>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</json:string></affiliations></json:item><json:item><name>Kristen M. Wilkes</name><affiliations><json:string>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</json:string></affiliations></json:item><json:item><name>Gregory Kapatos</name><affiliations><json:string>Department of Psychiatry and Behavioral Neurosciences and Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA</json:string></affiliations></json:item><json:item><name>John A. Hardy</name><affiliations><json:string>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</json:string></affiliations></json:item><json:item><name>Matt J. Farrer</name></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Article</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Loss-of-function mutations in the parkin gene were first identified in autosomal recessive juvenile parkinsonism (AR-JP). Subsequently, parkin mutations were found in many early-onset patients with Parkinson's disease (PD) (>45 years at onset). We hypothesized that parkin gene expression also may contribute to the age-associated risk of idiopathic PD (>50 years at onset). Two single-nucleotide polymorphisms within the parkin core promoter have been identified and assessed. We show one of the variants, −258 T/G, is located in a region of DNA that binds nuclear protein from human substantia nigra in vitro and functionally affects gene transcription. Furthermore, the −258 T/G polymorphism is genetically associated with idiopathic PD, as assessed in a large population-based series of cases and controls. Our results further implicate the parkin gene in the development of Parkinson's disease.</abstract><qualityIndicators><score>5.345</score><pdfVersion>1.2</pdfVersion><pdfPageSize>610 x 795 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>1</keywordCount><abstractCharCount>899</abstractCharCount><pdfWordCount>3785</pdfWordCount><pdfCharCount>24377</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>130</abstractWordCount></qualityIndicators><title>Functional association of the parkin gene promoter with idiopathic Parkinson's disease</title><genre><json:string>research-article</json:string></genre><host><volume>11</volume><pages><last>2792</last><first>2787</first></pages><issn><json:string>0964-6906</json:string></issn><issue>22</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>2002</publicationDate><copyrightDate>2002</copyrightDate><doi><json:string>10.1093/hmg/11.22.2787</json:string></doi><id>93538F48DC6955C6C824E588DE9A4352133D970B</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/93538F48DC6955C6C824E588DE9A4352133D970B/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/93538F48DC6955C6C824E588DE9A4352133D970B/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/93538F48DC6955C6C824E588DE9A4352133D970B/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Functional association of the parkin gene promoter with idiopathic Parkinson's disease</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>2002</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Functional association of the parkin gene promoter with idiopathic Parkinson's disease</title><author><persName><forename type="first">Andrew B.</forename><surname>West</surname></persName><affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</affiliation></author><author><persName><forename type="first">Demetrius</forename><surname>Maraganore</surname></persName><affiliation>Department of Neurology and</affiliation></author><author><persName><forename type="first">Julia</forename><surname>Crook</surname></persName><affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</affiliation></author><author><persName><forename type="first">Tim</forename><surname>Lesnick</surname></persName><affiliation>Division of Biostatistics, HSR, Mayo Clinic and Mayo Foundation, Rochester,MN 55905 USA and</affiliation></author><author><persName><forename type="first">Paul J.</forename><surname>Lockhart</surname></persName><affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</affiliation></author><author><persName><forename type="first">Kristen M.</forename><surname>Wilkes</surname></persName><affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</affiliation></author><author><persName><forename type="first">Gregory</forename><surname>Kapatos</surname></persName><affiliation>Department of Psychiatry and Behavioral Neurosciences and Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA</affiliation></author><author><persName><forename type="first">John A.</forename><surname>Hardy</surname></persName><affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</affiliation></author><author><persName><forename type="first">Matt J.</forename><surname>Farrer</surname></persName></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="2002-10-15"></date><biblScope unit="volume">11</biblScope><biblScope unit="issue">22</biblScope><biblScope unit="page" from="2787">2787</biblScope><biblScope unit="page" to="2792">2792</biblScope></imprint></monogr><idno type="istex">93538F48DC6955C6C824E588DE9A4352133D970B</idno><idno type="DOI">10.1093/hmg/11.22.2787</idno><idno type="local">ddf259</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2002</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Loss-of-function mutations in the parkin gene were first identified in autosomal recessive juvenile parkinsonism (AR-JP). Subsequently, parkin mutations were found in many early-onset patients with Parkinson's disease (PD) (<45 years at onset). We hypothesized that parkin gene expression also may contribute to the age-associated risk of idiopathic PD (>50 years at onset). Two single-nucleotide polymorphisms within the parkin core promoter have been identified and assessed. We show one of the variants, −258 T/G, is located in a region of DNA that binds nuclear protein from human substantia nigra in vitro and functionally affects gene transcription. Furthermore, the −258 T/G polymorphism is genetically associated with idiopathic PD, as assessed in a large population-based series of cases and controls. Our results further implicate the parkin gene in the development of Parkinson's disease.</p></abstract></profileDesc><revisionDesc><change when="2002-10-15">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-14">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/93538F48DC6955C6C824E588DE9A4352133D970B/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">ddf259</article-id><article-id pub-id-type="doi">10.1093/hmg/11.22.2787</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Functional association of the <italic>parkin</italic> gene promoter with idiopathic Parkinson's disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>West</surname><given-names>Andrew B.</given-names></name><xref rid="AF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Maraganore</surname><given-names>Demetrius</given-names></name><xref rid="AF2">2</xref></contrib><contrib contrib-type="author"><name><surname>Crook</surname><given-names>Julia</given-names></name><xref rid="AF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Lesnick</surname><given-names>Tim</given-names></name><xref rid="AF3">3</xref></contrib><contrib contrib-type="author"><name><surname>Lockhart</surname><given-names>Paul J.</given-names></name><xref rid="AF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Wilkes</surname><given-names>Kristen M.</given-names></name><xref rid="AF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Kapatos</surname><given-names>Gregory</given-names></name><xref rid="AF4">4</xref></contrib><contrib contrib-type="author"><name><surname>Hardy</surname><given-names>John A.</given-names></name><xref rid="AF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Farrer</surname><given-names>Matt J.</given-names></name><xref rid="FN1">*</xref></contrib><aff id="AF1"><sup>1</sup>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</aff><aff id="AF2"><sup>2</sup>Department of Neurology and</aff><aff id="AF3"><sup>3</sup>Division of Biostatistics, HSR, Mayo Clinic and Mayo Foundation, Rochester,MN 55905 USA and</aff><aff id="AF4"><sup>4</sup>Department of Psychiatry and Behavioral Neurosciences and Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA</aff></contrib-group><pub-date pub-type="ppub"><day>15</day><month>10</month><year>2002</year></pub-date><volume>11</volume><issue>22</issue><fpage>2787</fpage><lpage>2792</lpage><history><date date-type="accepted"><day>8</day><month>08</month><year>2002</year></date><date date-type="received"><day>4</day><month>07</month><year>2002</year></date></history><permissions><copyright-year>2002</copyright-year></permissions><abstract xml:lang="en"><p>Loss-of-function mutations in the <italic>parkin</italic> gene were first identified in autosomal recessive juvenile parkinsonism (AR-JP). Subsequently, <italic>parkin</italic> mutations were found in many early-onset patients with Parkinson's disease (PD) (<45 years at onset). We hypothesized that <italic>parkin</italic> gene expression also may contribute to the age-associated risk of idiopathic PD (>50 years at onset). Two single-nucleotide polymorphisms within the <italic>parkin</italic> core promoter have been identified and assessed. We show one of the variants, −258 T/G, is located in a region of DNA that binds nuclear protein from human substantia nigra <italic>in vitro</italic> and functionally affects gene transcription. Furthermore, the −258 T/G polymorphism is genetically associated with idiopathic PD, as assessed in a large population-based series of cases and controls. Our results further implicate the <italic>parkin</italic> gene in the development of Parkinson's disease.</p></abstract><custom-meta-wrap><custom-meta><meta-name>hwp-legacy-fpage</meta-name><meta-value>2787</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>Functional association of the parkin gene promoter with idiopathic Parkinson's disease</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Functional association of the parkin gene promoter with idiopathic Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Andrew B.</namePart><namePart type="family">West</namePart><affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Demetrius</namePart><namePart type="family">Maraganore</namePart><affiliation>Department of Neurology and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Julia</namePart><namePart type="family">Crook</namePart><affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tim</namePart><namePart type="family">Lesnick</namePart><affiliation>Division of Biostatistics, HSR, Mayo Clinic and Mayo Foundation, Rochester,MN 55905 USA and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paul J.</namePart><namePart type="family">Lockhart</namePart><affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kristen M.</namePart><namePart type="family">Wilkes</namePart><affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gregory</namePart><namePart type="family">Kapatos</namePart><affiliation>Department of Psychiatry and Behavioral Neurosciences and Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John A.</namePart><namePart type="family">Hardy</namePart><affiliation>Laboratories of Neurogenetics, Department of Neuroscience, Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Matt J.</namePart><namePart type="family">Farrer</namePart><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">2002-10-15</dateIssued><copyrightDate encoding="w3cdtf">2002</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">Loss-of-function mutations in the parkin gene were first identified in autosomal recessive juvenile parkinsonism (AR-JP). Subsequently, parkin mutations were found in many early-onset patients with Parkinson's disease (PD) (<45 years at onset). We hypothesized that parkin gene expression also may contribute to the age-associated risk of idiopathic PD (>50 years at onset). Two single-nucleotide polymorphisms within the parkin core promoter have been identified and assessed. We show one of the variants, −258 T/G, is located in a region of DNA that binds nuclear protein from human substantia nigra in vitro and functionally affects gene transcription. Furthermore, the −258 T/G polymorphism is genetically associated with idiopathic PD, as assessed in a large population-based series of cases and controls. Our results further implicate the parkin gene in the development of Parkinson's disease.</abstract><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>2002</date><detail type="volume"><caption>vol.</caption><number>11</number></detail><detail type="issue"><caption>no.</caption><number>22</number></detail><extent unit="pages"><start>2787</start><end>2792</end></extent></part></relatedItem><identifier type="istex">93538F48DC6955C6C824E588DE9A4352133D970B</identifier><identifier type="DOI">10.1093/hmg/11.22.2787</identifier><identifier type="local">ddf259</identifier><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/93538F48DC6955C6C824E588DE9A4352133D970B/annexes/jpeg</uri></json:item><json:item><original>true</original><mimetype>image/gif</mimetype><extension>gif</extension><uri>https://api.istex.fr/document/93538F48DC6955C6C824E588DE9A4352133D970B/annexes/gif</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/93538F48DC6955C6C824E588DE9A4352133D970B/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)
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