C‐terminal deletion mutant of MRE‐binding transcription factor‐1 inhibits MRE‐driven gene expression
Identifieur interne : 000010 ( Istex/Corpus ); précédent : 000009; suivant : 000011C‐terminal deletion mutant of MRE‐binding transcription factor‐1 inhibits MRE‐driven gene expression
Auteurs : Tomoki Kimura ; Norio Itoh ; Tomomichi Sone ; Keiichi Tanaka ; Masakazu IsobeSource :
- Journal of Cellular Biochemistry [ 0730-2312 ] ; 2004-10-15.
Abstract
Heavy metal‐induced transcriptional activation of the genes coding for metallothionein (MT) is mediated by a cis‐acting DNA element, the metal‐responsive element (MRE). MRE‐binding transcription factor‐1 (MTF‐1) is a highly conserved heavy metal‐induced transcriptional activator. MTF‐1 also activates transcription in response to oxidative stress and regulates the expression of several cytoprotective factor genes, including MT, γ‐glutamylcysteine synthetase, and Cu/Zn‐superoxide dismutase. It is thus thought that MTF‐1 plays a role in cellular stress response. The physiological role of MTF‐1 remains unclear because of the lack of MTF‐1‐specific activators and/or inhibitors. To obtain an MTF‐1‐specific inhibitor, we constructed an MTFΔC (amino acids 1–317), a C‐terminal deletion mutant of MTF‐1. MTFΔC could bind MRE and competed with MTF‐1 for MTF–MRE complex formation. Transient expression of MTFΔC in HepG2 cells reduced MRE‐driven gene expression, demonstrating that MTFΔC is dominant to MTF‐1. HepG2 cells stably expressing MTFΔC showed increased susceptibility to the cytotoxic effects of tert‐butyl hydroperoxide (tBH). Furthermore, we constructed Ad5MTFΔC, a recombinant adenovirus that expresses MTFΔC. Infection with the virus induced MTFΔC expression and increased susceptibility to the cytotoxic effects of tBH. These results indicate that MTF‐1 participates in controlling the cellular redox state. © 2004 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jcb.20210
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Cellular Biochemistry</title><title level="j" type="alt">JOURNAL OF CELLULAR BIOCHEMISTRY</title><idno type="ISSN">0730-2312</idno><idno type="eISSN">1097-4644</idno><imprint><biblScope unit="vol">93</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="609">609</biblScope><biblScope unit="page" to="618">618</biblScope><biblScope unit="page-count">10</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2004-10-15">2004-10-15</date></imprint><idno type="ISSN">0730-2312</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0730-2312</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Heavy metal‐induced transcriptional activation of the genes coding for metallothionein (MT) is mediated by a cis‐acting DNA element, the metal‐responsive element (MRE). MRE‐binding transcription factor‐1 (MTF‐1) is a highly conserved heavy metal‐induced transcriptional activator. MTF‐1 also activates transcription in response to oxidative stress and regulates the expression of several cytoprotective factor genes, including MT, γ‐glutamylcysteine synthetase, and Cu/Zn‐superoxide dismutase. It is thus thought that MTF‐1 plays a role in cellular stress response. The physiological role of MTF‐1 remains unclear because of the lack of MTF‐1‐specific activators and/or inhibitors. To obtain an MTF‐1‐specific inhibitor, we constructed an MTFΔC (amino acids 1–317), a C‐terminal deletion mutant of MTF‐1. MTFΔC could bind MRE and competed with MTF‐1 for MTF–MRE complex formation. Transient expression of MTFΔC in HepG2 cells reduced MRE‐driven gene expression, demonstrating that MTFΔC is dominant to MTF‐1. HepG2 cells stably expressing MTFΔC showed increased susceptibility to the cytotoxic effects of tert‐butyl hydroperoxide (tBH). Furthermore, we constructed Ad5MTFΔC, a recombinant adenovirus that expresses MTFΔC. Infection with the virus induced MTFΔC expression and increased susceptibility to the cytotoxic effects of tBH. 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MRE‐binding transcription factor‐1 (MTF‐1) is a highly conserved heavy metal‐induced transcriptional activator. MTF‐1 also activates transcription in response to oxidative stress and regulates the expression of several cytoprotective factor genes, including MT, γ‐glutamylcysteine synthetase, and Cu/Zn‐superoxide dismutase. It is thus thought that MTF‐1 plays a role in cellular stress response. The physiological role of MTF‐1 remains unclear because of the lack of MTF‐1‐specific activators and/or inhibitors. To obtain an MTF‐1‐specific inhibitor, we constructed an MTFΔC (amino acids 1–317), a C‐terminal deletion mutant of MTF‐1. MTFΔC could bind MRE and competed with MTF‐1 for MTF–MRE complex formation. Transient expression of MTFΔC in HepG2 cells reduced MRE‐driven gene expression, demonstrating that MTFΔC is dominant to MTF‐1. HepG2 cells stably expressing MTFΔC showed increased susceptibility to the cytotoxic effects of tert‐butyl hydroperoxide (tBH). Furthermore, we constructed Ad5MTFΔC, a recombinant adenovirus that expresses MTFΔC. Infection with the virus induced MTFΔC expression and increased susceptibility to the cytotoxic effects of tBH. These results indicate that MTF‐1 participates in controlling the cellular redox state. © 2004 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>9.12</score><pdfWordCount>4792</pdfWordCount><pdfCharCount>31296</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>10</pdfPageCount><pdfPageSize>592 x 789 pts</pdfPageSize><pdfWordsPerPage>479</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>194</abstractWordCount><abstractCharCount>1445</abstractCharCount><keywordCount>3</keywordCount></qualityIndicators><title>C‐terminal deletion mutant of MRE‐binding transcription factor‐1 inhibits MRE‐driven gene expression</title><pmid><json:string>15378601</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Journal of Cellular Biochemistry</title><language><json:string>unknown</json:string></language><doi><json:string>10.1002/(ISSN)1097-4644</json:string></doi><issn><json:string>0730-2312</json:string></issn><eissn><json:string>1097-4644</json:string></eissn><publisherId><json:string>JCB</json:string></publisherId><volume>93</volume><issue>3</issue><pages><first>609</first><last>618</last><total>10</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Article</value></json:item><json:item><value>Articles</value></json:item></subject></host><namedEntities><unitex><date><json:string>2004</json:string></date><geogName></geogName><orgName><json:string>Marligen Biosciences, Inc.</json:string><json:string>Japan Society for the Promotion of Science</json:string><json:string>Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University</json:string><json:string>Wiley-Liss, Inc.</json:string><json:string>Biochem</json:string><json:string>Wiley-Liss, Inc</json:string><json:string>Department of Toxicology, Faculty of Pharmaceutical Sciences, Setsunan University</json:string><json:string>Japan Abstract Heavy</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Tomoki Kimura</json:string><json:string>Assays</json:string></persName><placeName><json:string>Bad Wildbad</json:string><json:string>Cytotoxicity</json:string><json:string>Germany</json:string><json:string>Madison</json:string><json:string>Japan</json:string><json:string>Tokyo</json:string><json:string>WI</json:string><json:string>Osaka</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Radtke et al.</json:string><json:string>Moffatt and Denizeau, 1997</json:string><json:string>Chen et al., 1999</json:string><json:string>Saydam et al., 2001</json:string><json:string>Michalska and Choo, 1993</json:string><json:string>Brown et al., 1993, 1994</json:string><json:string>LaRochelle et al.</json:string><json:string>Vanacore et al., 2000</json:string><json:string>Gunes et al., 1998</json:string><json:string>Gunes et al.</json:string><json:string>Dalton et al. [1996]</json:string><json:string>Karin et al., 1985</json:string><json:string>Yoo et al., 1999</json:string><json:string>Masters et al., 1994</json:string><json:string>Iimuro et al., 1998</json:string><json:string>Radtke et al., 1995</json:string><json:string>Lichtlen et al., 2001</json:string><json:string>Heuchel et al., 1994</json:string><json:string>Kimura et al.</json:string><json:string>Bauman et al., 1991</json:string><json:string>Otsuka et al., 1994</json:string><json:string>LaRochelle et al., 2001</json:string><json:string>Beg et al., 1995</json:string><json:string>Vasak and Hasler, 2000</json:string><json:string>Stuart et al., 1985</json:string><json:string>Bittel et al., 1998</json:string><json:string>De et al., 1990</json:string><json:string>Smirnova et al., 2000</json:string><json:string>Sato et al., 1994, 1996</json:string><json:string>Ghoshal et al., 2002</json:string><json:string>Dalton et al., 1996, 1997a</json:string><json:string>Zhang and Hua, 2004</json:string><json:string>Dalton et al.</json:string><json:string>Radtke et al., 1993</json:string><json:string>Hilberg et al., 1993</json:string><json:string>Saydam et al., 2002</json:string><json:string>Mueller et al., 1988</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-FZ1BJN6C-L</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - cell biology</json:string><json:string>2 - biochemistry & molecular biology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - biochemistry & molecular biology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Cell Biology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular 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xml:id="author-0004"><persName><forename type="first">Masakazu</forename><surname>Isobe</surname></persName><affiliation><orgName type="department">Department of Toxicology</orgName><orgName type="department">Faculty of Pharmaceutical Sciences</orgName><orgName type="institution">Setsunan University</orgName><address><addrLine>45‐1 Nagaotoge‐cho</addrLine><addrLine>Hirakata, Osaka 573‐0101, Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><idno type="istex">A5D650FCFE61BC7ADBCA4ACF2459B5CBD947DF52</idno><idno type="ark">ark:/67375/WNG-FZ1BJN6C-L</idno><idno type="DOI">10.1002/jcb.20210</idno><idno type="unit">JCB20210</idno><idno type="toTypesetVersion">file:JCB.JCB20210.pdf</idno></analytic><monogr><title level="j" type="main">Journal of Cellular Biochemistry</title><title level="j" type="alt">JOURNAL OF CELLULAR BIOCHEMISTRY</title><idno type="pISSN">0730-2312</idno><idno type="eISSN">1097-4644</idno><idno 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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><p>Heavy metal‐induced transcriptional activation of the genes coding for metallothionein (MT) is mediated by a <hi rend="italic">cis</hi>‐acting DNA element, the metal‐responsive element (MRE). MRE‐binding transcription factor‐1 (MTF‐1) is a highly conserved heavy metal‐induced transcriptional activator. MTF‐1 also activates transcription in response to oxidative stress and regulates the expression of several cytoprotective factor genes, including MT, γ‐glutamylcysteine synthetase, and Cu/Zn‐superoxide dismutase. It is thus thought that MTF‐1 plays a role in cellular stress response. The physiological role of MTF‐1 remains unclear because of the lack of MTF‐1‐specific activators and/or inhibitors. To obtain an MTF‐1‐specific inhibitor, we constructed an MTFΔC (amino acids 1–317), a C‐terminal deletion mutant of MTF‐1. MTFΔC could bind MRE and competed with MTF‐1 for MTF–MRE complex formation. Transient expression of MTFΔC in HepG2 cells reduced MRE‐driven gene expression, demonstrating that MTFΔC is dominant to MTF‐1. HepG2 cells stably expressing MTFΔC showed increased susceptibility to the cytotoxic effects of <hi rend="italic">tert</hi>‐butyl hydroperoxide (<hi rend="italic">t</hi>BH). Furthermore, we constructed Ad5MTFΔC, a recombinant adenovirus that expresses MTFΔC. Infection with the virus induced MTFΔC expression and increased susceptibility to the cytotoxic effects of <hi rend="italic">t</hi>BH. These results indicate that MTF‐1 participates in controlling the cellular redox state. © 2004 Wiley‐Liss, Inc.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="kwd1">MRE‐binding transcription factor‐1</term><term xml:id="kwd2">dominant‐negative mutant</term><term xml:id="kwd3">oxidative stress</term></keywords><keywords rend="articleCategory"><term>Article</term></keywords><keywords rend="tocHeading1"><term>Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-FZ1BJN6C-L/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>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1097-4644</doi><issn type="print">0730-2312</issn><issn type="electronic">1097-4644</issn><idGroup><id type="product" value="JCB"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF CELLULAR BIOCHEMISTRY">Journal of Cellular Biochemistry</title><title type="short">J. Cell. Biochem.</title></titleGroup></publicationMeta><publicationMeta level="part" position="30"><doi origin="wiley" registered="yes">10.1002/jcb.v93:3</doi><numberingGroup><numbering type="journalVolume" number="93">93</numbering><numbering type="journalIssue">3</numbering></numberingGroup><coverDate startDate="2004-10-15">15 October 2004</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="17" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jcb.20210</doi><idGroup><id type="unit" value="JCB20210"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2004 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2004-01-28"></event><event type="manuscriptAccepted" date="2004-05-10"></event><event type="publishedOnlineEarlyUnpaginated" date="2004-08-11"></event><event type="firstOnline" date="2004-08-11"></event><event type="publishedOnlineFinalForm" date="2004-09-15"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-06"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-29"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-24"></event></eventGroup><numberingGroup><numbering type="pageFirst">609</numbering><numbering type="pageLast">618</numbering></numberingGroup><correspondenceTo>Department of Toxicology, Faculty of Pharmaceutical Sciences, Setsunan University, 45‐1 Nagaotoge‐cho, Hirakata, Osaka 573‐0101, Japan.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JCB.JCB20210.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="6"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="39"></count><count type="wordTotal" number="5258"></count></countGroup><titleGroup><title type="main" xml:lang="en">C‐terminal deletion mutant of MRE‐binding transcription factor‐1 inhibits MRE‐driven gene expression</title><title type="short" xml:lang="en">Inhibition of MTF‐1 by Its Deletion Mutant</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>Tomoki</givenNames><familyName>Kimura</familyName></personName><contactDetails><email>tomoki@pharm.setsunan.ac.jp</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Norio</givenNames><familyName>Itoh</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Tomomichi</givenNames><familyName>Sone</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Keiichi</givenNames><familyName>Tanaka</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Masakazu</givenNames><familyName>Isobe</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="JP" type="organization"><unparsedAffiliation>Department of Toxicology, Faculty of Pharmaceutical Sciences, Setsunan University, 45‐1 Nagaotoge‐cho, Hirakata, Osaka 573‐0101, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="JP" type="organization"><unparsedAffiliation>Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University, 1‐6, Yamada‐oka, Suita, Osaka 565‐0871, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">MRE‐binding transcription factor‐1</keyword><keyword xml:id="kwd2">dominant‐negative mutant</keyword><keyword xml:id="kwd3">oxidative stress</keyword></keywordGroup><fundingInfo><fundingAgency>Japan Society for the Promotion of Science</fundingAgency><fundingNumber>15790080</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Heavy metal‐induced transcriptional activation of the genes coding for metallothionein (MT) is mediated by a <i>cis</i>‐acting DNA element, the metal‐responsive element (MRE). MRE‐binding transcription factor‐1 (MTF‐1) is a highly conserved heavy metal‐induced transcriptional activator. MTF‐1 also activates transcription in response to oxidative stress and regulates the expression of several cytoprotective factor genes, including MT, γ‐glutamylcysteine synthetase, and Cu/Zn‐superoxide dismutase. It is thus thought that MTF‐1 plays a role in cellular stress response. The physiological role of MTF‐1 remains unclear because of the lack of MTF‐1‐specific activators and/or inhibitors. To obtain an MTF‐1‐specific inhibitor, we constructed an MTFΔC (amino acids 1–317), a C‐terminal deletion mutant of MTF‐1. MTFΔC could bind MRE and competed with MTF‐1 for MTF–MRE complex formation. Transient expression of MTFΔC in HepG2 cells reduced MRE‐driven gene expression, demonstrating that MTFΔC is dominant to MTF‐1. HepG2 cells stably expressing MTFΔC showed increased susceptibility to the cytotoxic effects of <i>tert</i>‐butyl hydroperoxide (<i>t</i>BH). Furthermore, we constructed Ad5MTFΔC, a recombinant adenovirus that expresses MTFΔC. Infection with the virus induced MTFΔC expression and increased susceptibility to the cytotoxic effects of <i>t</i>BH. These results indicate that MTF‐1 participates in controlling the cellular redox state. © 2004 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>C‐terminal deletion mutant of MRE‐binding transcription factor‐1 inhibits MRE‐driven gene expression</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Inhibition of MTF‐1 by Its Deletion Mutant</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>C‐terminal deletion mutant of MRE‐binding transcription factor‐1 inhibits MRE‐driven gene expression</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="given">Tomoki</namePart><namePart type="family">Kimura</namePart><affiliation>Department of Toxicology, Faculty of Pharmaceutical Sciences, Setsunan University, 45‐1 Nagaotoge‐cho, Hirakata, Osaka 573‐0101, Japan</affiliation><affiliation>E-mail: tomoki@pharm.setsunan.ac.jp</affiliation><affiliation>Correspondence address: Department of Toxicology, Faculty of Pharmaceutical Sciences, Setsunan University, 45‐1 Nagaotoge‐cho, Hirakata, Osaka 573‐0101, Japan.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Norio</namePart><namePart type="family">Itoh</namePart><affiliation>Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University, 1‐6, Yamada‐oka, Suita, Osaka 565‐0871, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tomomichi</namePart><namePart type="family">Sone</namePart><affiliation>Department of Toxicology, Faculty of Pharmaceutical Sciences, Setsunan University, 45‐1 Nagaotoge‐cho, Hirakata, Osaka 573‐0101, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Keiichi</namePart><namePart type="family">Tanaka</namePart><affiliation>Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University, 1‐6, Yamada‐oka, Suita, Osaka 565‐0871, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Masakazu</namePart><namePart type="family">Isobe</namePart><affiliation>Department of Toxicology, Faculty of Pharmaceutical Sciences, Setsunan University, 45‐1 Nagaotoge‐cho, Hirakata, Osaka 573‐0101, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2004-10-15</dateIssued><dateCaptured encoding="w3cdtf">2004-01-28</dateCaptured><dateValid encoding="w3cdtf">2004-05-10</dateValid><copyrightDate encoding="w3cdtf">2004</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">6</extent><extent unit="tables">0</extent><extent unit="references">39</extent><extent unit="words">5258</extent></physicalDescription><abstract lang="en">Heavy metal‐induced transcriptional activation of the genes coding for metallothionein (MT) is mediated by a cis‐acting DNA element, the metal‐responsive element (MRE). MRE‐binding transcription factor‐1 (MTF‐1) is a highly conserved heavy metal‐induced transcriptional activator. MTF‐1 also activates transcription in response to oxidative stress and regulates the expression of several cytoprotective factor genes, including MT, γ‐glutamylcysteine synthetase, and Cu/Zn‐superoxide dismutase. It is thus thought that MTF‐1 plays a role in cellular stress response. The physiological role of MTF‐1 remains unclear because of the lack of MTF‐1‐specific activators and/or inhibitors. To obtain an MTF‐1‐specific inhibitor, we constructed an MTFΔC (amino acids 1–317), a C‐terminal deletion mutant of MTF‐1. MTFΔC could bind MRE and competed with MTF‐1 for MTF–MRE complex formation. Transient expression of MTFΔC in HepG2 cells reduced MRE‐driven gene expression, demonstrating that MTFΔC is dominant to MTF‐1. HepG2 cells stably expressing MTFΔC showed increased susceptibility to the cytotoxic effects of tert‐butyl hydroperoxide (tBH). Furthermore, we constructed Ad5MTFΔC, a recombinant adenovirus that expresses MTFΔC. Infection with the virus induced MTFΔC expression and increased susceptibility to the cytotoxic effects of tBH. These results indicate that MTF‐1 participates in controlling the cellular redox state. © 2004 Wiley‐Liss, Inc.</abstract><note type="funding">Japan Society for the Promotion of Science - No. 15790080; </note><subject lang="en"><genre>keywords</genre><topic>MRE‐binding transcription factor‐1</topic><topic>dominant‐negative mutant</topic><topic>oxidative stress</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Cellular Biochemistry</title></titleInfo><titleInfo type="abbreviated"><title>J. Cell. Biochem.</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>article-category</genre><topic>Article</topic><topic>Articles</topic></subject><identifier type="ISSN">0730-2312</identifier><identifier type="eISSN">1097-4644</identifier><identifier type="DOI">10.1002/(ISSN)1097-4644</identifier><identifier type="PublisherID">JCB</identifier><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>93</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>609</start><end>618</end><total>10</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>Increase in metallothionein produced by chemicals that induce oxidative stress</title></titleInfo><name type="personal"><namePart type="given">JW</namePart><namePart type="family">Bauman</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Liu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YP</namePart><namePart type="family">Liu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CD</namePart><namePart type="family">Klaassen</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Bauman JW, Liu J, Liu YP, Klaassen CD. 1991. Increase in metallothionein produced by chemicals that induce oxidative stress. Toxicol Appl Pharmacol 110: 347–354.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>110</number></detail><extent unit="pages"><start>347</start><end>354</end></extent></part><relatedItem type="host"><titleInfo><title>Toxicol Appl Pharmacol</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>110</number></detail><extent unit="pages"><start>347</start><end>354</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit2"><titleInfo><title>Embryonic lethality and liver degeneration in mice lacking the RelA component of NF‐kappa B</title></titleInfo><name type="personal"><namePart type="given">AA</namePart><namePart type="family">Beg</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">WC</namePart><namePart type="family">Sha</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RT</namePart><namePart type="family">Bronson</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Ghosh</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Baltimore</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Beg AA, Sha WC, Bronson RT, Ghosh S, Baltimore D. 1995. Embryonic lethality and liver degeneration in mice lacking the RelA component of NF‐kappa B. Nature 376: 167–170.</note><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>376</number></detail><extent unit="pages"><start>167</start><end>170</end></extent></part><relatedItem type="host"><titleInfo><title>Nature</title></titleInfo><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>376</number></detail><extent unit="pages"><start>167</start><end>170</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit3"><titleInfo><title>The DNA binding activity of metal response element‐binding transcription factor‐1 is activated in vivo and in vitro by zinc, but not by other transition metals</title></titleInfo><name type="personal"><namePart type="given">D</namePart><namePart type="family">Bittel</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Dalton</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SL</namePart><namePart type="family">Samson</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Gedamu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GK</namePart><namePart type="family">Andrews</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Bittel D, Dalton T, Samson SL, Gedamu L, Andrews GK. 1998. The DNA binding activity of metal response element‐binding transcription factor‐1 is activated in vivo and in vitro by zinc, but not by other transition metals. J Biol Chem 273: 7127–7133.</note><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>273</number></detail><extent unit="pages"><start>7127</start><end>7133</end></extent></part><relatedItem type="host"><titleInfo><title>J Biol Chem</title></titleInfo><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>273</number></detail><extent unit="pages"><start>7127</start><end>7133</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit4"><titleInfo><title>Suppression of oncogene‐induced transformation by a deletion mutant of c‐jun</title></titleInfo><name type="personal"><namePart type="given">PH</namePart><namePart type="family">Brown</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Alani</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LH</namePart><namePart type="family">Preis</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Szabo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MJ</namePart><namePart type="family">Birrer</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Brown PH, Alani R, Preis LH, Szabo E, Birrer MJ. 1993. Suppression of oncogene‐induced transformation by a deletion mutant of c‐jun. Oncogene 8: 877–886.</note><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><extent unit="pages"><start>877</start><end>886</end></extent></part><relatedItem type="host"><titleInfo><title>Oncogene</title></titleInfo><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><extent unit="pages"><start>877</start><end>886</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit5"><titleInfo><title>Mechanism of action of a dominant‐negative mutant of c‐Jun</title></titleInfo><name type="personal"><namePart type="given">PH</namePart><namePart type="family">Brown</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">TK</namePart><namePart type="family">Chen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MJ</namePart><namePart type="family">Birrer</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Brown PH, Chen TK, Birrer MJ. 1994. Mechanism of action of a dominant‐negative mutant of c‐Jun. Oncogene 9: 791–799.</note><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>791</start><end>799</end></extent></part><relatedItem type="host"><titleInfo><title>Oncogene</title></titleInfo><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>791</start><end>799</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit6"><titleInfo><title>MRE‐Binding transcription factor‐1: Weak zinc‐binding finger domains 5 and 6 modulate the structure, affinity, and specificity of the metal‐response element complex</title></titleInfo><name type="personal"><namePart type="given">X</namePart><namePart type="family">Chen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Chu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DP</namePart><namePart type="family">Giedroc</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Chen X, Chu M, Giedroc DP. 1999. MRE‐Binding transcription factor‐1: Weak zinc‐binding finger domains 5 and 6 modulate the structure, affinity, and specificity of the metal‐response element complex. Biochemistry 38: 12915–12925.</note><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>38</number></detail><extent unit="pages"><start>12915</start><end>12925</end></extent></part><relatedItem type="host"><titleInfo><title>Biochemistry</title></titleInfo><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>38</number></detail><extent unit="pages"><start>12915</start><end>12925</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit7"><titleInfo><title>Oxidative stress activates metal‐responsive transcription factor‐1 binding activity. Occupancy in vivo of metal response elements in the metallothionein‐I gene promoter</title></titleInfo><name type="personal"><namePart type="given">TP</namePart><namePart type="family">Dalton</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Q</namePart><namePart type="family">Li</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Bittel</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Liang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GK</namePart><namePart type="family">Andrews</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Dalton TP, Li Q, Bittel D, Liang L, Andrews GK. 1996. Oxidative stress activates metal‐responsive transcription factor‐1 binding activity. Occupancy in vivo of metal response elements in the metallothionein‐I gene promoter. J Biol Chem 271: 26233–26241.</note><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>271</number></detail><extent unit="pages"><start>26233</start><end>26241</end></extent></part><relatedItem type="host"><titleInfo><title>J Biol Chem</title></titleInfo><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>271</number></detail><extent unit="pages"><start>26233</start><end>26241</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit8"><titleInfo><title>Activation of the chicken metallothionein promoter by metals and oxidative stress in cultured cells and transgenic mice</title></titleInfo><name type="personal"><namePart type="given">T</namePart><namePart type="family">Dalton</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">BC</namePart><namePart type="family">Paria</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LP</namePart><namePart type="family">Fernando</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YM</namePart><namePart type="family">Huet‐Hudson</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SK</namePart><namePart type="family">Dey</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GK</namePart><namePart type="family">Andrews</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Dalton T, Paria BC, Fernando LP, Huet‐Hudson YM, Dey SK, Andrews GK. 1997a. Activation of the chicken metallothionein promoter by metals and oxidative stress in cultured cells and transgenic mice. Comp Biochem Physiol B Biochem Mol Biol 116: 75–86.</note><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>116</number></detail><extent unit="pages"><start>75</start><end>86</end></extent></part><relatedItem type="host"><titleInfo><title>Comp Biochem Physiol B Biochem Mol Biol</title></titleInfo><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>116</number></detail><extent unit="pages"><start>75</start><end>86</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit9"><titleInfo><title>Reversible activation of mouse metal response element‐binding transcription factor 1 DNA binding involves zinc interaction with the zinc finger domain</title></titleInfo><name type="personal"><namePart type="given">TP</namePart><namePart type="family">Dalton</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Bittel</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GK</namePart><namePart type="family">Andrews</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Dalton TP, Bittel D, Andrews GK. 1997b. Reversible activation of mouse metal response element‐binding transcription factor 1 DNA binding involves zinc interaction with the zinc finger domain. Mol Cell Biol 17: 2781–2789.</note><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>2781</start><end>2789</end></extent></part><relatedItem type="host"><titleInfo><title>Mol Cell Biol</title></titleInfo><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>2781</start><end>2789</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit10"><titleInfo><title>Endotoxin induction of murine metallothionein gene expression</title></titleInfo><name type="personal"><namePart type="given">SK</namePart><namePart type="family">De</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MT</namePart><namePart type="family">McMaster</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GK</namePart><namePart type="family">Andrews</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">De SK, McMaster MT, Andrews GK. 1990. Endotoxin induction of murine metallothionein gene expression. J Biol Chem 265: 15267–15274.</note><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>265</number></detail><extent unit="pages"><start>15267</start><end>15274</end></extent></part><relatedItem type="host"><titleInfo><title>J Biol Chem</title></titleInfo><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>265</number></detail><extent unit="pages"><start>15267</start><end>15274</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit11"><titleInfo><title>Inhibitors of histone deacetylase and DNA methyltransferase synergistically activate the methylated metallothionein I promoter by activating the transcription factor MTF‐1 and forming an open chromatin structure</title></titleInfo><name type="personal"><namePart type="given">K</namePart><namePart type="family">Ghoshal</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Datta</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Majumder</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Bai</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">X</namePart><namePart type="family">Dong</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Parthun</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ST</namePart><namePart type="family">Jacob</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Ghoshal K, Datta J, Majumder S, Bai S, Dong X, Parthun M, Jacob ST. 2002. Inhibitors of histone deacetylase and DNA methyltransferase synergistically activate the methylated metallothionein I promoter by activating the transcription factor MTF‐1 and forming an open chromatin structure. Mol Cell Biol 22: 8302–8319.</note><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><extent unit="pages"><start>8302</start><end>8319</end></extent></part><relatedItem type="host"><titleInfo><title>Mol Cell Biol</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><extent unit="pages"><start>8302</start><end>8319</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit12"><titleInfo><title>Embryonic lethality and liver degeneration in mice lacking the metal‐responsive transcriptional activator MTF‐1</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Gunes</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Heuchel</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O</namePart><namePart type="family">Georgiev</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KH</namePart><namePart type="family">Muller</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Lichtlen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Bluthmann</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Marino</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Aguzzi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Schaffner</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Gunes C, Heuchel R, Georgiev O, Muller KH, Lichtlen P, Bluthmann H, Marino S, Aguzzi A, Schaffner W. 1998. Embryonic lethality and liver degeneration in mice lacking the metal‐responsive transcriptional activator MTF‐1. EMBO J 17: 2846–2854.</note><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>2846</start><end>2854</end></extent></part><relatedItem type="host"><titleInfo><title>EMBO J</title></titleInfo><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>2846</start><end>2854</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit13"><titleInfo><title>Metallothionein</title></titleInfo><name type="personal"><namePart type="given">DH</namePart><namePart type="family">Hamer</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Hamer DH. 1986. Metallothionein. Annu Rev Biochem 55: 913–951.</note><part><date>1986</date><detail type="volume"><caption>vol.</caption><number>55</number></detail><extent unit="pages"><start>913</start><end>951</end></extent></part><relatedItem type="host"><titleInfo><title>Annu Rev Biochem</title></titleInfo><part><date>1986</date><detail type="volume"><caption>vol.</caption><number>55</number></detail><extent unit="pages"><start>913</start><end>951</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit14"><titleInfo><title>The transcription factor MTF‐1 is essential for basal and heavy metal‐induced metallothionein gene expression</title></titleInfo><name type="personal"><namePart type="given">R</namePart><namePart type="family">Heuchel</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Radtke</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O</namePart><namePart type="family">Georgiev</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Stark</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Aguet</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Schaffner</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Heuchel R, Radtke F, Georgiev O, Stark G, Aguet M, Schaffner W. 1994. The transcription factor MTF‐1 is essential for basal and heavy metal‐induced metallothionein gene expression. EMBO J 13: 2870–2875.</note><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>2870</start><end>2875</end></extent></part><relatedItem type="host"><titleInfo><title>EMBO J</title></titleInfo><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>2870</start><end>2875</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit15"><titleInfo><title>c‐jun is essential for normal mouse development and hepatogenesis</title></titleInfo><name type="personal"><namePart type="given">F</namePart><namePart type="family">Hilberg</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Aguzzi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Howells</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">EF</namePart><namePart type="family">Wagner</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Hilberg F, Aguzzi A, Howells N, Wagner EF. 1993. c‐jun is essential for normal mouse development and hepatogenesis. Nature 365: 179–181.</note><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>365</number></detail><extent unit="pages"><start>179</start><end>181</end></extent></part><relatedItem type="host"><titleInfo><title>Nature</title></titleInfo><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>365</number></detail><extent unit="pages"><start>179</start><end>181</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit16"><titleInfo><title>NFkappaB prevents apoptosis and liver dysfunction during liver regeneration</title></titleInfo><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Iimuro</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Nishiura</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Hellerbrand</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KE</namePart><namePart type="family">Behrns</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Schoonhoven</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JW</namePart><namePart type="family">Grisham</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DA</namePart><namePart type="family">Brenner</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Iimuro Y, Nishiura T, Hellerbrand C, Behrns KE, Schoonhoven R, Grisham JW, Brenner DA. 1998. NFkappaB prevents apoptosis and liver dysfunction during liver regeneration. J Clin Invest 101: 802–811.</note><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>101</number></detail><extent unit="pages"><start>802</start><end>811</end></extent></part><relatedItem type="host"><titleInfo><title>J Clin Invest</title></titleInfo><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>101</number></detail><extent unit="pages"><start>802</start><end>811</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit17"><titleInfo><title>Interleukin 1 regulates human metallothionein gene expression</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Karin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RJ</namePart><namePart type="family">Imbra</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Heguy</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Wong</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Karin M, Imbra RJ, Heguy A, Wong G. 1985. Interleukin 1 regulates human metallothionein gene expression. Mol Cell Biol 5: 2866–2869.</note><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>5</number></detail><extent unit="pages"><start>2866</start><end>2869</end></extent></part><relatedItem type="host"><titleInfo><title>Mol Cell Biol</title></titleInfo><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>5</number></detail><extent unit="pages"><start>2866</start><end>2869</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit18"><titleInfo><title>Phosphorylation is involved in the activation of metal‐regulatory transcription factor 1 in response to metal ions</title></titleInfo><name type="personal"><namePart type="given">O</namePart><namePart type="family">LaRochelle</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">V</namePart><namePart type="family">Gagne</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Charron</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JW</namePart><namePart type="family">Soh</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Seguin</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">LaRochelle O, Gagne V, Charron J, Soh JW, Seguin C. 2001. Phosphorylation is involved in the activation of metal‐regulatory transcription factor 1 in response to metal ions. J Biol Chem 276: 41879–41888.</note><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>276</number></detail><extent unit="pages"><start>41879</start><end>41888</end></extent></part><relatedItem type="host"><titleInfo><title>J Biol Chem</title></titleInfo><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>276</number></detail><extent unit="pages"><start>41879</start><end>41888</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit19"><titleInfo><title>Target gene search for the metal‐responsive transcription factor MTF‐1</title></titleInfo><name type="personal"><namePart type="given">P</namePart><namePart type="family">Lichtlen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Wang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Belser</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O</namePart><namePart type="family">Georgiev</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">U</namePart><namePart type="family">Certa</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Sack</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Schaffner</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Lichtlen P, Wang Y, Belser T, Georgiev O, Certa U, Sack R, Schaffner W. 2001. Target gene search for the metal‐responsive transcription factor MTF‐1. Nucleic Acids Res 29: 1514–1523.</note><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>29</number></detail><extent unit="pages"><start>1514</start><end>1523</end></extent></part><relatedItem type="host"><titleInfo><title>Nucleic Acids Res</title></titleInfo><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>29</number></detail><extent unit="pages"><start>1514</start><end>1523</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit20"><titleInfo><title>Targeted disruption of metallothionein I and II genes increases sensitivity to cadmium</title></titleInfo><name type="personal"><namePart type="given">BA</namePart><namePart type="family">Masters</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">EJ</namePart><namePart type="family">Kelly</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CJ</namePart><namePart type="family">Quaife</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RL</namePart><namePart type="family">Brinster</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RD</namePart><namePart type="family">Palmiter</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Masters BA, Kelly EJ, Quaife CJ, Brinster RL, Palmiter RD. 1994. Targeted disruption of metallothionein I and II genes increases sensitivity to cadmium. Proc Natl Acad Sci USA 91: 584–588.</note><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>91</number></detail><extent unit="pages"><start>584</start><end>588</end></extent></part><relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title></titleInfo><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>91</number></detail><extent unit="pages"><start>584</start><end>588</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit21"><titleInfo><title>Targeting and germ‐line transmission of a null mutation at the metallothionein I and II loci in mouse</title></titleInfo><name type="personal"><namePart type="given">AE</namePart><namePart type="family">Michalska</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KH</namePart><namePart type="family">Choo</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Michalska AE, Choo KH. 1993. Targeting and germ‐line transmission of a null mutation at the metallothionein I and II loci in mouse. Proc Natl Acad Sci USA 90: 8088–8092.</note><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>90</number></detail><extent unit="pages"><start>8088</start><end>8092</end></extent></part><relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title></titleInfo><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>90</number></detail><extent unit="pages"><start>8088</start><end>8092</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit22"><titleInfo><title>Metallothionein in physiological and physiopathological processes</title></titleInfo><name type="personal"><namePart type="given">P</namePart><namePart type="family">Moffatt</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Denizeau</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Moffatt P, Denizeau F. 1997. Metallothionein in physiological and physiopathological processes. Drug Metab Rev 29: 261–307.</note><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>29</number></detail><extent unit="pages"><start>261</start><end>307</end></extent></part><relatedItem type="host"><titleInfo><title>Drug Metab Rev</title></titleInfo><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>29</number></detail><extent unit="pages"><start>261</start><end>307</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit23"><titleInfo><title>Rapid colorimetric assay for cellular growth and survival: Application to proliferation and cytotoxicity assays</title></titleInfo><name type="personal"><namePart type="given">T</namePart><namePart type="family">Mosmann</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Mosmann T. 1983. Rapid colorimetric assay for cellular growth and survival: Application to proliferation and cytotoxicity assays. J Immunol Methods 65: 55–63.</note><part><date>1983</date><detail type="volume"><caption>vol.</caption><number>65</number></detail><extent unit="pages"><start>55</start><end>63</end></extent></part><relatedItem type="host"><titleInfo><title>J Immunol Methods</title></titleInfo><part><date>1983</date><detail type="volume"><caption>vol.</caption><number>65</number></detail><extent unit="pages"><start>55</start><end>63</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit24"><titleInfo><title>Constitutive and metal‐inducible protein:DNA interactions at the mouse metallothionein I promoter examined by in vivo and in vitro footprinting</title></titleInfo><name type="personal"><namePart type="given">PR</namePart><namePart type="family">Mueller</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SJ</namePart><namePart type="family">Salser</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Wold</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Mueller PR, Salser SJ, Wold B. 1988. Constitutive and metal‐inducible protein:DNA interactions at the mouse metallothionein I promoter examined by in vivo and in vitro footprinting. Genes Dev 2: 412–427.</note><part><date>1988</date><detail type="volume"><caption>vol.</caption><number>2</number></detail><extent unit="pages"><start>412</start><end>427</end></extent></part><relatedItem type="host"><titleInfo><title>Genes Dev</title></titleInfo><part><date>1988</date><detail type="volume"><caption>vol.</caption><number>2</number></detail><extent unit="pages"><start>412</start><end>427</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit25"><titleInfo><title>Optimization of experimental variables influencing reporter gene expression in hepatoma cells following calcium phosphate transfection</title></titleInfo><name type="personal"><namePart type="given">JV</namePart><namePart type="family">O'Mahoney</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">TE</namePart><namePart type="family">Adams</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">O'Mahoney JV, Adams TE. 1994. Optimization of experimental variables influencing reporter gene expression in hepatoma cells following calcium phosphate transfection. DNA Cell Biol 13: 1227–1232.</note><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>1227</start><end>1232</end></extent></part><relatedItem type="host"><titleInfo><title>DNA Cell Biol</title></titleInfo><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>1227</start><end>1232</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit26"><titleInfo><title>Purification and characterization of a protein that binds to metal responsive elements of the human metallothionein IIA gene</title></titleInfo><name type="personal"><namePart type="given">F</namePart><namePart type="family">Otsuka</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Iwamatsu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Suzuki</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Ohsawa</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DH</namePart><namePart type="family">Hamer</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Koizumi</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Otsuka F, Iwamatsu A, Suzuki K, Ohsawa M, Hamer DH, Koizumi S. 1994. Purification and characterization of a protein that binds to metal responsive elements of the human metallothionein IIA gene. J Biol Chem 269: 23700–23707.</note><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>269</number></detail><extent unit="pages"><start>23700</start><end>23707</end></extent></part><relatedItem type="host"><titleInfo><title>J Biol Chem</title></titleInfo><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>269</number></detail><extent unit="pages"><start>23700</start><end>23707</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit27"><titleInfo><title>Cloned transcription factor MTF‐1 activates the mouse metallothionein I promoter</title></titleInfo><name type="personal"><namePart type="given">F</namePart><namePart type="family">Radtke</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Heuchel</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O</namePart><namePart type="family">Georgiev</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Hergersberg</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Gariglio</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Z</namePart><namePart type="family">Dembic</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Schaffner</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Radtke F, Heuchel R, Georgiev O, Hergersberg M, Gariglio M, Dembic Z, Schaffner W. 1993. Cloned transcription factor MTF‐1 activates the mouse metallothionein I promoter. EMBO J 12: 1355–1362.</note><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>12</number></detail><extent unit="pages"><start>1355</start><end>1362</end></extent></part><relatedItem type="host"><titleInfo><title>EMBO J</title></titleInfo><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>12</number></detail><extent unit="pages"><start>1355</start><end>1362</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit28"><titleInfo><title>Functional domains of the heavy metal‐responsive transcription regulator MTF‐1</title></titleInfo><name type="personal"><namePart type="given">F</namePart><namePart type="family">Radtke</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O</namePart><namePart type="family">Georgiev</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HP</namePart><namePart type="family">Muller</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Brugnera</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Schaffner</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Radtke F, Georgiev O, Muller HP, Brugnera E, Schaffner W. 1995. Functional domains of the heavy metal‐responsive transcription regulator MTF‐1. Nucleic Acids Res 23: 2277–2286.</note><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><extent unit="pages"><start>2277</start><end>2286</end></extent></part><relatedItem type="host"><titleInfo><title>Nucleic Acids Res</title></titleInfo><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><extent unit="pages"><start>2277</start><end>2286</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit29"><titleInfo><title>Dose‐dependent increases in metallothionein synthesis in the lung and liver of paraquat‐treated rats</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Sato</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Sato M. 1991. Dose‐dependent increases in metallothionein synthesis in the lung and liver of paraquat‐treated rats. Toxicol Appl Pharmacol 107: 98–105.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>107</number></detail><extent unit="pages"><start>98</start><end>105</end></extent></part><relatedItem type="host"><titleInfo><title>Toxicol Appl Pharmacol</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>107</number></detail><extent unit="pages"><start>98</start><end>105</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit30"><titleInfo><title>Differential induction of metallothionein synthesis by interleukin‐6 and tumor necrosis factor‐alpha in rat tissues</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Sato</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Sasaki</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Hojo</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Sato M, Sasaki M, Hojo H. 1994. Differential induction of metallothionein synthesis by interleukin‐6 and tumor necrosis factor‐alpha in rat tissues. Int J Immunopharmacol 16: 187–195.</note><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><extent unit="pages"><start>187</start><end>195</end></extent></part><relatedItem type="host"><titleInfo><title>Int J Immunopharmacol</title></titleInfo><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><extent unit="pages"><start>187</start><end>195</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit31"><titleInfo><title>Metallothionein synthesis induced by interferon alpha/beta in mice of various zinc status</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Sato</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Yamaki</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Oguro</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Yoshida</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Nomura</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Nakajima</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Sato M, Yamaki J, Oguro T, Yoshida T, Nomura N, Nakajima K. 1996. Metallothionein synthesis induced by interferon alpha/beta in mice of various zinc status. Tohoku J Exp Med 178: 241–250.</note><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>178</number></detail><extent unit="pages"><start>241</start><end>250</end></extent></part><relatedItem type="host"><titleInfo><title>Tohoku J Exp Med</title></titleInfo><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>178</number></detail><extent unit="pages"><start>241</start><end>250</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit32"><titleInfo><title>Nucleo‐cytoplasmic trafficking of metal‐regulatory transcription factor 1 is regulated by diverse stress signals</title></titleInfo><name type="personal"><namePart type="given">N</namePart><namePart type="family">Saydam</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O</namePart><namePart type="family">Georgiev</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MY</namePart><namePart type="family">Nakano</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">UF</namePart><namePart type="family">Greber</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Schaffner</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Saydam N, Georgiev O, Nakano MY, Greber UF, Schaffner W. 2001. Nucleo‐cytoplasmic trafficking of metal‐regulatory transcription factor 1 is regulated by diverse stress signals. J Biol Chem 276: 25487–25495.</note><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>276</number></detail><extent unit="pages"><start>25487</start><end>25495</end></extent></part><relatedItem type="host"><titleInfo><title>J Biol Chem</title></titleInfo><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>276</number></detail><extent unit="pages"><start>25487</start><end>25495</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit33"><titleInfo><title>Regulation of metallothionein transcription by the metal‐responsive transcription factor MTF‐1: Identification of signal transduction cascades that control metal‐inducible transcription</title></titleInfo><name type="personal"><namePart type="given">N</namePart><namePart type="family">Saydam</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">TK</namePart><namePart type="family">Adams</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Steiner</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Schaffner</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JH</namePart><namePart type="family">Freedman</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Saydam N, Adams TK, Steiner F, Schaffner W, Freedman JH. 2002. Regulation of metallothionein transcription by the metal‐responsive transcription factor MTF‐1: Identification of signal transduction cascades that control metal‐inducible transcription. J Biol Chem 277: 20438–20445.</note><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>277</number></detail><extent unit="pages"><start>20438</start><end>20445</end></extent></part><relatedItem type="host"><titleInfo><title>J Biol Chem</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>277</number></detail><extent unit="pages"><start>20438</start><end>20445</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit34"><titleInfo><title>Zinc and cadmium can promote rapid nuclear translocation of metal response element‐binding transcription factor‐1</title></titleInfo><name type="personal"><namePart type="given">IV</namePart><namePart type="family">Smirnova</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DC</namePart><namePart type="family">Bittel</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Ravindra</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Jiang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GK</namePart><namePart type="family">Andrews</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Smirnova IV, Bittel DC, Ravindra R, Jiang H, Andrews GK. 2000. Zinc and cadmium can promote rapid nuclear translocation of metal response element‐binding transcription factor‐1. J Biol Chem 275: 9377–9384.</note><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>275</number></detail><extent unit="pages"><start>9377</start><end>9384</end></extent></part><relatedItem type="host"><titleInfo><title>J Biol Chem</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>275</number></detail><extent unit="pages"><start>9377</start><end>9384</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit35"><titleInfo><title>Identification of multiple metal regulatory elements in mouse metallothionein‐I promoter by assaying synthetic sequences</title></titleInfo><name type="personal"><namePart type="given">GW</namePart><namePart type="family">Stuart</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PF</namePart><namePart type="family">Searle</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RD</namePart><namePart type="family">Palmiter</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Stuart GW, Searle PF, Palmiter RD. 1985. Identification of multiple metal regulatory elements in mouse metallothionein‐I promoter by assaying synthetic sequences. Nature 317: 828–831.</note><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>317</number></detail><extent unit="pages"><start>828</start><end>831</end></extent></part><relatedItem type="host"><titleInfo><title>Nature</title></titleInfo><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>317</number></detail><extent unit="pages"><start>828</start><end>831</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit36"><titleInfo><title>Role for copper in transient oxidation and nuclear translocation of MTF‐1, but not of NF‐kappa B, by the heme‐hemopexin transport system</title></titleInfo><name type="personal"><namePart type="given">RM</namePart><namePart type="family">Vanacore</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JD</namePart><namePart type="family">Eskew</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PJ</namePart><namePart type="family">Morales</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Sung</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Smith</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Vanacore RM, Eskew JD, Morales PJ, Sung L, Smith A. 2000. Role for copper in transient oxidation and nuclear translocation of MTF‐1, but not of NF‐kappa B, by the heme‐hemopexin transport system. Antioxid Redox Signal 2: 739–752.</note><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>2</number></detail><extent unit="pages"><start>739</start><end>752</end></extent></part><relatedItem type="host"><titleInfo><title>Antioxid Redox Signal</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>2</number></detail><extent unit="pages"><start>739</start><end>752</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit37"><titleInfo><title>Metallothioneins: New functional and structural insights</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Vasak</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DW</namePart><namePart type="family">Hasler</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Vasak M, Hasler DW. 2000. Metallothioneins: New functional and structural insights. Curr Opin Chem Biol 4: 177–183.</note><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>177</start><end>183</end></extent></part><relatedItem type="host"><titleInfo><title>Curr Opin Chem Biol</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>177</start><end>183</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit38"><titleInfo><title>Heavy metal‐mediated activation of the rat Cu/Zn superoxide dismutase gene via a metal‐responsive element</title></titleInfo><name type="personal"><namePart type="given">HY</namePart><namePart type="family">Yoo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MS</namePart><namePart type="family">Chang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HM</namePart><namePart type="family">Rho</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Yoo HY, Chang MS, Rho HM. 1999. Heavy metal‐mediated activation of the rat Cu/Zn superoxide dismutase gene via a metal‐responsive element. Mol Gen Genet 262: 310–313.</note><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>262</number></detail><extent unit="pages"><start>310</start><end>313</end></extent></part><relatedItem type="host"><titleInfo><title>Mol Gen Genet</title></titleInfo><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>262</number></detail><extent unit="pages"><start>310</start><end>313</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit39"><titleInfo><title>Targeted gene silencing by small interfering RNA‐based knock‐down technology</title></titleInfo><name type="personal"><namePart type="given">J</namePart><namePart type="family">Zhang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ZC</namePart><namePart type="family">Hua</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Zhang J, Hua ZC. 2004. Targeted gene silencing by small interfering RNA‐based knock‐down technology. Curr Pharm Biotechnol 5: 1–7.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>5</number></detail><extent unit="pages"><start>1</start><end>7</end></extent></part><relatedItem type="host"><titleInfo><title>Curr Pharm Biotechnol</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>5</number></detail><extent unit="pages"><start>1</start><end>7</end></extent></part></relatedItem></relatedItem><identifier type="istex">A5D650FCFE61BC7ADBCA4ACF2459B5CBD947DF52</identifier><identifier type="ark">ark:/67375/WNG-FZ1BJN6C-L</identifier><identifier type="DOI">10.1002/jcb.20210</identifier><identifier type="ArticleID">JCB20210</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2004 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Converted from (version ) to MODS version 3.6.</recordOrigin><recordCreationDate encoding="w3cdtf">2019-11-15</recordCreationDate></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-FZ1BJN6C-L/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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