Corticosterone Actions on the Hippocampal Brain‐Derived Neurotrophic Factor Expression are Mediated by Exon IV Promoter
Identifieur interne : 001339 ( Main/Corpus ); précédent : 001338; suivant : 001340Corticosterone Actions on the Hippocampal Brain‐Derived Neurotrophic Factor Expression are Mediated by Exon IV Promoter
Auteurs : A. C. Hansson ; W. H. Sommer ; M. Metsis ; I. Strömberg ; L. F. Agnati ; K. FuxeSource :
- Journal of Neuroendocrinology [ 0953-8194 ] ; 2006-02.
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- KwdEn :
Abstract
Brain‐derived neurotrophic factor (BDNF) expression is strongly regulated by adrenocorticosteroids via activated gluco‐ and mineralocorticoid receptors. Four separate promoters are located upstream of the BDNF noncoding exons I to IV and may thus be involved in adrenocorticosteroid‐mediated gene regulation. In adrenalectomised rats, corticosterone (10 mg/kg s.c.) induces a robust down‐regulation of both BDNF mRNA and protein levels in the hippocampus peaking at 2–8 h. To study the role of the individual promoters in the corticosterone response, we employed exon‐specific riboprobe in situ hybridisation as well as real‐time polymerase chain reaction (PCR) in the dentate gyrus. We found a down‐regulation, mainly of exon IV and the protein‐coding exon V, in nearby all hippocampal subregions, but exon II was only down‐regulated in the dentate gyrus. Exon I and exon III transcripts were not affected by corticosterone treatment. The results could be confirmed with real‐time PCR in the dentate gyrus. It appears as if the exon IV promoter is the major target for corticosterone‐mediated transcriptional regulation of BDNF in the hippocampus.
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DOI: 10.1111/j.1365-2826.2005.01390.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Corticosterone Actions on the Hippocampal Brain‐Derived Neurotrophic Factor Expression are Mediated by Exon IV Promoter</title><author><name sortKey="Hansson, A C" sort="Hansson, A C" uniqKey="Hansson A" first="A. C." last="Hansson">A. C. Hansson</name><affiliation><mods:affiliation>Departments of Neuroscience</mods:affiliation></affiliation><affiliation><mods:affiliation>Laboratory of Clinical Science, NIAAA, Bethesda, USA.</mods:affiliation></affiliation></author><author><name sortKey="Sommer, W H" sort="Sommer, W H" uniqKey="Sommer W" first="W. H." last="Sommer">W. H. Sommer</name><affiliation><mods:affiliation>Laboratory of Clinical Science, NIAAA, Bethesda, USA.</mods:affiliation></affiliation></author><author><name sortKey="Metsis, M" sort="Metsis, M" uniqKey="Metsis M" first="M." last="Metsis">M. Metsis</name><affiliation><mods:affiliation>Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.</mods:affiliation></affiliation></author><author><name sortKey="Stromberg, I" sort="Stromberg, I" uniqKey="Stromberg I" first="I." last="Strömberg">I. Strömberg</name><affiliation><mods:affiliation>Department of Integrative Medical Biology, Umeå University, Umeå, Sweden.</mods:affiliation></affiliation></author><author><name sortKey="Agnati, L F" sort="Agnati, L F" uniqKey="Agnati L" first="L. F." last="Agnati">L. F. Agnati</name><affiliation><mods:affiliation>Department of Biomedical Science, University of Modena, Modena, Italy.</mods:affiliation></affiliation></author><author><name sortKey="Fuxe, K" sort="Fuxe, K" uniqKey="Fuxe K" first="K." last="Fuxe">K. 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Hansson</name><affiliation><mods:affiliation>Departments of Neuroscience</mods:affiliation></affiliation><affiliation><mods:affiliation>Laboratory of Clinical Science, NIAAA, Bethesda, USA.</mods:affiliation></affiliation></author><author><name sortKey="Sommer, W H" sort="Sommer, W H" uniqKey="Sommer W" first="W. H." last="Sommer">W. H. Sommer</name><affiliation><mods:affiliation>Laboratory of Clinical Science, NIAAA, Bethesda, USA.</mods:affiliation></affiliation></author><author><name sortKey="Metsis, M" sort="Metsis, M" uniqKey="Metsis M" first="M." last="Metsis">M. Metsis</name><affiliation><mods:affiliation>Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.</mods:affiliation></affiliation></author><author><name sortKey="Stromberg, I" sort="Stromberg, I" uniqKey="Stromberg I" first="I." last="Strömberg">I. 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Fuxe</name><affiliation><mods:affiliation>Departments of Neuroscience</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neuroendocrinology</title><idno type="ISSN">0953-8194</idno><idno type="eISSN">1365-2826</idno><imprint><publisher>Blackwell Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2006-02">2006-02</date><biblScope unit="volume">18</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="104">104</biblScope><biblScope unit="page" to="114">114</biblScope></imprint><idno type="ISSN">0953-8194</idno></series><idno type="istex">12C2AA8F8B35815765B26F0722896515F175321C</idno><idno type="DOI">10.1111/j.1365-2826.2005.01390.x</idno><idno type="ArticleID">JNE1390</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0953-8194</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>adrenalectomy</term><term>brain‐derived neurotrophic factor</term><term>glucocorticoids</term><term>neurotrophin</term><term>rat brain</term><term>rat brain neurotrophin</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Brain‐derived neurotrophic factor (BDNF) expression is strongly regulated by adrenocorticosteroids via activated gluco‐ and mineralocorticoid receptors. Four separate promoters are located upstream of the BDNF noncoding exons I to IV and may thus be involved in adrenocorticosteroid‐mediated gene regulation. In adrenalectomised rats, corticosterone (10 mg/kg s.c.) induces a robust down‐regulation of both BDNF mRNA and protein levels in the hippocampus peaking at 2–8 h. To study the role of the individual promoters in the corticosterone response, we employed exon‐specific riboprobe in situ hybridisation as well as real‐time polymerase chain reaction (PCR) in the dentate gyrus. We found a down‐regulation, mainly of exon IV and the protein‐coding exon V, in nearby all hippocampal subregions, but exon II was only down‐regulated in the dentate gyrus. Exon I and exon III transcripts were not affected by corticosterone treatment. The results could be confirmed with real‐time PCR in the dentate gyrus. It appears as if the exon IV promoter is the major target for corticosterone‐mediated transcriptional regulation of BDNF in the hippocampus.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>A. C. Hansson</name><affiliations><json:string>Departments of Neuroscience</json:string><json:string>Laboratory of Clinical Science, NIAAA, Bethesda, USA.</json:string></affiliations></json:item><json:item><name>W. H. Sommer</name><affiliations><json:string>Laboratory of Clinical Science, NIAAA, Bethesda, USA.</json:string></affiliations></json:item><json:item><name>M. Metsis</name><affiliations><json:string>Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.</json:string></affiliations></json:item><json:item><name>I. Strömberg</name><affiliations><json:string>Department of Integrative Medical Biology, Umeå University, Umeå, Sweden.</json:string></affiliations></json:item><json:item><name>L. F. Agnati</name><affiliations><json:string>Department of Biomedical Science, University of Modena, Modena, Italy.</json:string></affiliations></json:item><json:item><name>K. 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Four separate promoters are located upstream of the BDNF noncoding exons I to IV and may thus be involved in adrenocorticosteroid‐mediated gene regulation. In adrenalectomised rats, corticosterone (10 mg/kg s.c.) induces a robust down‐regulation of both BDNF mRNA and protein levels in the hippocampus peaking at 2–8 h. To study the role of the individual promoters in the corticosterone response, we employed exon‐specific riboprobe in situ hybridisation as well as real‐time polymerase chain reaction (PCR) in the dentate gyrus. We found a down‐regulation, mainly of exon IV and the protein‐coding exon V, in nearby all hippocampal subregions, but exon II was only down‐regulated in the dentate gyrus. Exon I and exon III transcripts were not affected by corticosterone treatment. The results could be confirmed with real‐time PCR in the dentate gyrus. 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C.</forename><surname>Hansson</surname></persName><affiliation>Departments of Neuroscience</affiliation><affiliation>Laboratory of Clinical Science, NIAAA, Bethesda, USA.</affiliation></author><author><persName><forename type="first">W. H.</forename><surname>Sommer</surname></persName><affiliation>Laboratory of Clinical Science, NIAAA, Bethesda, USA.</affiliation></author><author><persName><forename type="first">M.</forename><surname>Metsis</surname></persName><affiliation>Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.</affiliation></author><author><persName><forename type="first">I.</forename><surname>Strömberg</surname></persName><affiliation>Department of Integrative Medical Biology, Umeå University, Umeå, Sweden.</affiliation></author><author><persName><forename type="first">L. F.</forename><surname>Agnati</surname></persName><affiliation>Department of Biomedical Science, University of Modena, Modena, Italy.</affiliation></author><author><persName><forename type="first">K.</forename><surname>Fuxe</surname></persName><affiliation>Departments of Neuroscience</affiliation></author></analytic><monogr><title level="j">Journal of Neuroendocrinology</title><idno type="pISSN">0953-8194</idno><idno type="eISSN">1365-2826</idno><idno type="DOI">10.1111/(ISSN)1365-2826</idno><imprint><publisher>Blackwell Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2006-02"></date><biblScope unit="volume">18</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="104">104</biblScope><biblScope unit="page" to="114">114</biblScope></imprint></monogr><idno type="istex">12C2AA8F8B35815765B26F0722896515F175321C</idno><idno type="DOI">10.1111/j.1365-2826.2005.01390.x</idno><idno type="ArticleID">JNE1390</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2006</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Brain‐derived neurotrophic factor (BDNF) expression is strongly regulated by adrenocorticosteroids via activated gluco‐ and mineralocorticoid receptors. Four separate promoters are located upstream of the BDNF noncoding exons I to IV and may thus be involved in adrenocorticosteroid‐mediated gene regulation. In adrenalectomised rats, corticosterone (10 mg/kg s.c.) induces a robust down‐regulation of both BDNF mRNA and protein levels in the hippocampus peaking at 2–8 h. To study the role of the individual promoters in the corticosterone response, we employed exon‐specific riboprobe in situ hybridisation as well as real‐time polymerase chain reaction (PCR) in the dentate gyrus. We found a down‐regulation, mainly of exon IV and the protein‐coding exon V, in nearby all hippocampal subregions, but exon II was only down‐regulated in the dentate gyrus. Exon I and exon III transcripts were not affected by corticosterone treatment. The results could be confirmed with real‐time PCR in the dentate gyrus. It appears as if the exon IV promoter is the major target for corticosterone‐mediated transcriptional regulation of BDNF in the hippocampus.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>neurotrophin</term></item><item><term>brain‐derived neurotrophic factor</term></item><item><term>adrenalectomy</term></item><item><term>glucocorticoids</term></item><item><term>rat brain neurotrophin</term></item><item><term>brain‐derived neurotrophic factor</term></item><item><term>adrenalectomy</term></item><item><term>glucocorticoids</term></item><item><term>rat brain</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-02">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/12C2AA8F8B35815765B26F0722896515F175321C/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Science Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1365-2826</doi><issn type="print">0953-8194</issn><issn type="electronic">1365-2826</issn><idGroup><id type="product" value="JNE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="JOURNAL OF NEUROENDOCRINOLOGY">Journal of Neuroendocrinology</title></titleGroup></publicationMeta><publicationMeta level="part" position="02002"><doi origin="wiley">10.1111/jne.2006.18.issue-2</doi><numberingGroup><numbering type="journalVolume" number="18">18</numbering><numbering type="journalIssue" number="2">2</numbering></numberingGroup><coverDate startDate="2006-02">February 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="3" status="forIssue"><doi origin="wiley">10.1111/j.1365-2826.2005.01390.x</doi><idGroup><id type="unit" value="JNE1390"></id></idGroup><countGroup><count type="pageTotal" number="11"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><eventGroup><event type="firstOnline" date="2005-11-09"></event><event type="publishedOnlineFinalForm" date="2005-12-15"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-16"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-31"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-30"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="104">104</numbering><numbering type="pageLast" number="114">114</numbering></numberingGroup><correspondenceTo>Dr Anita C. Hansson, NIAAA, NIH, Building 10, CRC, Room 1‐5330 (East), 10 Center Drive MSC 1108, Bethesda, MD 20892‐1108, USA (e‐mail: <email>anita.hansson@mail.nih.gov</email>).</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JNE.JNE1390.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted 18 October 2005</unparsedEditorialHistory><countGroup><count type="figureTotal" number="8"></count><count type="tableTotal" number="2"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="58"></count><count type="wordTotal" number="6460"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Corticosterone Actions on the Hippocampal Brain‐Derived Neurotrophic Factor Expression are Mediated by Exon IV Promoter</title><title type="short">Corticosterone actions on the hippocampal BDNF expression</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2"><personName><givenNames>A. C.</givenNames><familyName>Hansson</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>W. H.</givenNames><familyName>Sommer</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a3"><personName><givenNames>M.</givenNames><familyName>Metsis</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a4"><personName><givenNames>I.</givenNames><familyName>Strömberg</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a5"><personName><givenNames>L. F.</givenNames><familyName>Agnati</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>K.</givenNames><familyName>Fuxe</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Departments of Neuroscience</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="SE"><unparsedAffiliation>Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Laboratory of Clinical Science, NIAAA, Bethesda, USA.</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="SE"><unparsedAffiliation>Department of Integrative Medical Biology, Umeå University, Umeå, Sweden.</unparsedAffiliation></affiliation><affiliation xml:id="a5" countryCode="IT"><unparsedAffiliation>Department of Biomedical Science, University of Modena, Modena, Italy.</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">neurotrophin</keyword><keyword xml:id="k2">brain‐derived neurotrophic factor</keyword><keyword xml:id="k3">adrenalectomy</keyword><keyword xml:id="k4">glucocorticoids</keyword><keyword xml:id="k5">rat brain neurotrophin</keyword><keyword xml:id="k6">brain‐derived neurotrophic factor</keyword><keyword xml:id="k7">adrenalectomy</keyword><keyword xml:id="k8">glucocorticoids</keyword><keyword xml:id="k9">rat brain</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Brain‐derived neurotrophic factor (BDNF) expression is strongly regulated by adrenocorticosteroids via activated gluco‐ and mineralocorticoid receptors. Four separate promoters are located upstream of the BDNF noncoding exons I to IV and may thus be involved in adrenocorticosteroid‐mediated gene regulation. In adrenalectomised rats, corticosterone (10 mg/kg s.c.) induces a robust down‐regulation of both BDNF mRNA and protein levels in the hippocampus peaking at 2–8 h. To study the role of the individual promoters in the corticosterone response, we employed exon‐specific riboprobe <i>in situ</i> hybridisation as well as real‐time polymerase chain reaction (PCR) in the dentate gyrus. We found a down‐regulation, mainly of exon IV and the protein‐coding exon V, in nearby all hippocampal subregions, but exon II was only down‐regulated in the dentate gyrus. Exon I and exon III transcripts were not affected by corticosterone treatment. The results could be confirmed with real‐time PCR in the dentate gyrus. It appears as if the exon IV promoter is the major target for corticosterone‐mediated transcriptional regulation of BDNF in the hippocampus.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Corticosterone Actions on the Hippocampal Brain‐Derived Neurotrophic Factor Expression are Mediated by Exon IV Promoter</title></titleInfo><titleInfo type="abbreviated"><title>Corticosterone actions on the hippocampal BDNF expression</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Corticosterone Actions on the Hippocampal Brain‐Derived Neurotrophic Factor Expression are Mediated by Exon IV Promoter</title></titleInfo><name type="personal"><namePart type="given">A. 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H.</namePart><namePart type="family">Sommer</namePart><affiliation>Laboratory of Clinical Science, NIAAA, Bethesda, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Metsis</namePart><affiliation>Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I.</namePart><namePart type="family">Strömberg</namePart><affiliation>Department of Integrative Medical Biology, Umeå University, Umeå, Sweden.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L. F.</namePart><namePart type="family">Agnati</namePart><affiliation>Department of Biomedical Science, University of Modena, Modena, Italy.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Fuxe</namePart><affiliation>Departments of Neuroscience</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Science Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2006-02</dateIssued><edition>Accepted 18 October 2005</edition><copyrightDate encoding="w3cdtf">2006</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">8</extent><extent unit="tables">2</extent><extent unit="references">58</extent><extent unit="words">6460</extent></physicalDescription><abstract lang="en">Brain‐derived neurotrophic factor (BDNF) expression is strongly regulated by adrenocorticosteroids via activated gluco‐ and mineralocorticoid receptors. Four separate promoters are located upstream of the BDNF noncoding exons I to IV and may thus be involved in adrenocorticosteroid‐mediated gene regulation. In adrenalectomised rats, corticosterone (10 mg/kg s.c.) induces a robust down‐regulation of both BDNF mRNA and protein levels in the hippocampus peaking at 2–8 h. To study the role of the individual promoters in the corticosterone response, we employed exon‐specific riboprobe in situ hybridisation as well as real‐time polymerase chain reaction (PCR) in the dentate gyrus. We found a down‐regulation, mainly of exon IV and the protein‐coding exon V, in nearby all hippocampal subregions, but exon II was only down‐regulated in the dentate gyrus. Exon I and exon III transcripts were not affected by corticosterone treatment. The results could be confirmed with real‐time PCR in the dentate gyrus. It appears as if the exon IV promoter is the major target for corticosterone‐mediated transcriptional regulation of BDNF in the hippocampus.</abstract><subject lang="en"><genre>Keywords</genre><topic>neurotrophin</topic><topic>brain‐derived neurotrophic factor</topic><topic>adrenalectomy</topic><topic>glucocorticoids</topic><topic>rat brain neurotrophin</topic><topic>brain‐derived neurotrophic factor</topic><topic>adrenalectomy</topic><topic>glucocorticoids</topic><topic>rat brain</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neuroendocrinology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0953-8194</identifier><identifier type="eISSN">1365-2826</identifier><identifier type="DOI">10.1111/(ISSN)1365-2826</identifier><identifier type="PublisherID">JNE</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>104</start><end>114</end><total>11</total></extent></part></relatedItem><identifier type="istex">12C2AA8F8B35815765B26F0722896515F175321C</identifier><identifier type="DOI">10.1111/j.1365-2826.2005.01390.x</identifier><identifier type="ArticleID">JNE1390</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Science Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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