GAL4 activates gene expression in mammalian cells
Identifieur interne : 001736 ( Istex/Corpus ); précédent : 001735; suivant : 001737GAL4 activates gene expression in mammalian cells
Auteurs : Hitoshi Kakidani ; Mark PtashneSource :
- Cell [ 0092-8674 ] ; 1988.
English descriptors
- Teeft :
- 1fmer, Activates, Activates gene expression, Activates transcription, Activator, Amino, Amino acids, Biol, Deletion, Deletion derivatives, Derivative, Dexamethasone, Effector, Effector plasmid, Effector plasmids, Gal4, Gal4 binding site, Galactose, Gene expression, Giniger, Glucocorticoid, Glucocorticoid receptor, Gres, Late promoter, Mammalian cells, Mmtv, Mmtv promoter, Pgmcs, Plasmid, Promoter, Ptashne, Receptor, Reference plasmid, Reporter plasmid, Reporter plasmids, Transcription, Transcriptional, Transfected, Tumor virus, Uaso, Yamamoto, Yeast.
Abstract
Abstract: GAL4, a protein that activates transcription in yeast, is shown to activate the mouse mammary tumor virus promoter in mammalian cells. Activation depends upon a GAL4-binding sequence inserted upstream of the gene. Deletion mutants of GAL4 bearing one or both of the “activating regions” required for activation in yeast also activate transcription in mammalian cells. A derivative of GAL4 that binds to DNA but cannot activate transcription in yeast also fails to activate transcription in mammalian cells. We also show that GAL4 and the glucocorticoid receptor activate the mouse mammary tumor virus promoter synergistically.
Url:
DOI: 10.1016/0092-8674(88)90504-1
Links to Exploration step
ISTEX:4ED3863029916E163B658E0C5218BD04C07FE3D9Le document en format XML
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Activation depends upon a GAL4-binding sequence inserted upstream of the gene. Deletion mutants of GAL4 bearing one or both of the “activating regions” required for activation in yeast also activate transcription in mammalian cells. A derivative of GAL4 that binds to DNA but cannot activate transcription in yeast also fails to activate transcription in mammalian cells. We also show that GAL4 and the glucocorticoid receptor activate the mouse mammary tumor virus promoter synergistically.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>gal4</json:string><json:string>plasmid</json:string><json:string>ptashne</json:string><json:string>promoter</json:string><json:string>transcriptional</json:string><json:string>mmtv</json:string><json:string>gres</json:string><json:string>uaso</json:string><json:string>effector</json:string><json:string>mmtv promoter</json:string><json:string>mammalian cells</json:string><json:string>activates</json:string><json:string>receptor</json:string><json:string>glucocorticoid</json:string><json:string>yamamoto</json:string><json:string>transfected</json:string><json:string>giniger</json:string><json:string>derivative</json:string><json:string>activator</json:string><json:string>reporter plasmid</json:string><json:string>1fmer</json:string><json:string>biol</json:string><json:string>pgmcs</json:string><json:string>transcription</json:string><json:string>galactose</json:string><json:string>deletion</json:string><json:string>gene expression</json:string><json:string>activates transcription</json:string><json:string>yeast</json:string><json:string>tumor virus</json:string><json:string>gal4 binding site</json:string><json:string>glucocorticoid receptor</json:string><json:string>amino acids</json:string><json:string>effector plasmid</json:string><json:string>reporter plasmids</json:string><json:string>dexamethasone</json:string><json:string>amino</json:string><json:string>late promoter</json:string><json:string>activates gene expression</json:string><json:string>effector plasmids</json:string><json:string>reference plasmid</json:string><json:string>deletion derivatives</json:string></teeft></keywords><author><json:item><name>Hitoshi Kakidani</name><affiliations><json:string>Department of Biochemistry and Molecular Biology Harvard University Cambridge, Massachusetts 02138 USA</json:string></affiliations></json:item><json:item><name>Mark Ptashne</name><affiliations><json:string>Department of Biochemistry and Molecular Biology Harvard University Cambridge, Massachusetts 02138 USA</json:string></affiliations></json:item></author><arkIstex>ark:/67375/6H6-NPHVWCR4-D</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: GAL4, a protein that activates transcription in yeast, is shown to activate the mouse mammary tumor virus promoter in mammalian cells. Activation depends upon a GAL4-binding sequence inserted upstream of the gene. Deletion mutants of GAL4 bearing one or both of the “activating regions” required for activation in yeast also activate transcription in mammalian cells. A derivative of GAL4 that binds to DNA but cannot activate transcription in yeast also fails to activate transcription in mammalian cells. We also show that GAL4 and the glucocorticoid receptor activate the mouse mammary tumor virus promoter synergistically.</abstract><qualityIndicators><score>7.218</score><pdfWordCount>4078</pdfWordCount><pdfCharCount>26887</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>619.56 x 799.28 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>95</abstractWordCount><abstractCharCount>636</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>GAL4 activates gene expression in mammalian cells</title><pmid><json:string>2830021</json:string></pmid><pii><json:string>0092-8674(88)90504-1</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc. Natl. Acad. Sci. USA</title><language><json:string>unknown</json:string></language><volume>82</volume><pages><first>43</first><last>47</last></pages></serie><host><title>Cell</title><language><json:string>unknown</json:string></language><publicationDate>1988</publicationDate><issn><json:string>0092-8674</json:string></issn><pii><json:string>S0092-8674(00)X0420-5</json:string></pii><volume>52</volume><issue>2</issue><pages><first>161</first><last>167</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>35S</json:string><json:string>1988</json:string></date><geogName></geogName><orgName><json:string>Research Laboratory, Kanagawa</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>F. Baas</json:string><json:string>K. Yamamoto</json:string></persName><placeName><json:string>Okayama</json:string><json:string>Japan</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>see Gluzman, 1981</json:string><json:string>Ma and Ptashne, 1987a</json:string><json:string>Chandler et al., 1983</json:string><json:string>Giniger and Ptashne (1987)</json:string><json:string>Yocum et al., 1984</json:string><json:string>Giniger et al., 1985</json:string><json:string>Miesfeld et al., 1986</json:string><json:string>Brent and Ptashne, 1985</json:string><json:string>Scheidereit et al., 1983</json:string><json:string>Johnston et al., 1987</json:string><json:string>Southern and Berg, 1982</json:string><json:string>Gorman et al. (1982)</json:string><json:string>Yamamoto, 1985</json:string><json:string>Giniger and Ptashne, 1988</json:string><json:string>Gill and Ptashne, 1987</json:string><json:string>Brent and Ptashne, 1984</json:string><json:string>Mlfeld et al., 1986</json:string><json:string>Kaufman et al., 1985</json:string><json:string>Johnston and Davis, 1984</json:string><json:string>Charnay et al. (1984)</json:string><json:string>Cordingley et al., 1987</json:string><json:string>Chirgwin et al. (1979)</json:string><json:string>Zinn et al. (1983)</json:string><json:string>Gorman et al., 1982</json:string><json:string>Buetti and Diggelmann, 1993</json:string><json:string>Majors and Varmus, 1983</json:string><json:string>Webster et al. (1988)</json:string><json:string>Nowock et al., 1985</json:string><json:string>Struhl, 1987</json:string><json:string>Guarente et al., 1982</json:string><json:string>Karin et al., 1984</json:string><json:string>Oshima, 1982</json:string><json:string>Keegan et al., 1986</json:string><json:string>Jantzen et al., 1987</json:string><json:string>Ptashne, 1999</json:string><json:string>Hope and Struhl, 1988</json:string><json:string>Ma and Ptashne, 1987c</json:string><json:string>Kuhl et al. (1987)</json:string><json:string>Sawadogo and Roeder, 1985</json:string><json:string>Perlman and Hopper, 1979</json:string><json:string>Miksicek et al., 1986</json:string><json:string>Renkawitz et al., 1984</json:string><json:string>Ma and Ptashne, 1987b</json:string><json:string>Bram and Kornberg, 1985</json:string><json:string>Bonthron et al., 1986</json:string><json:string>Slater et al., 1985</json:string><json:string>West et al., 1984</json:string><json:string>Reinberg et al., 1987</json:string><json:string>Guarante et al. (1982)</json:string><json:string>Payvar et al., 1983</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-NPHVWCR4-D</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 - developmental 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 - General Biochemistry, Genetics and Molecular Biology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences biologiques fondamentales et appliquees. psychologie</json:string></inist></categories><publicationDate>1988</publicationDate><copyrightDate>1988</copyrightDate><doi><json:string>10.1016/0092-8674(88)90504-1</json:string></doi><id>4ED3863029916E163B658E0C5218BD04C07FE3D9</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-NPHVWCR4-D/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-NPHVWCR4-D/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-NPHVWCR4-D/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">GAL4 activates gene expression in mammalian cells</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>elsevier</p></licence></availability><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M"></p><date>1988</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note type="content">Section title: Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">GAL4 activates gene expression in mammalian cells</title><author xml:id="author-0000"><persName><forename type="first">Hitoshi</forename><surname>Kakidani</surname></persName><note type="biography">Present address: Biotechnology Research Laboratory, Tosoh Corporation, 2743-1 Hayakawa, Ayase, Kanagawa, Japan.</note><affiliation>Present address: Biotechnology Research Laboratory, Tosoh Corporation, 2743-1 Hayakawa, Ayase, Kanagawa, Japan.</affiliation><affiliation>Department of Biochemistry and Molecular Biology Harvard University Cambridge, Massachusetts 02138 USA</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Mark</forename><surname>Ptashne</surname></persName><affiliation>Department of Biochemistry and Molecular Biology Harvard University Cambridge, Massachusetts 02138 USA</affiliation></author><idno type="istex">4ED3863029916E163B658E0C5218BD04C07FE3D9</idno><idno type="ark">ark:/67375/6H6-NPHVWCR4-D</idno><idno type="DOI">10.1016/0092-8674(88)90504-1</idno><idno type="PII">0092-8674(88)90504-1</idno></analytic><monogr><title level="j">Cell</title><title level="j" type="abbrev">CELL</title><idno type="pISSN">0092-8674</idno><idno type="PII">S0092-8674(00)X0420-5</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1988"></date><biblScope unit="volume">52</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="161">161</biblScope><biblScope unit="page" to="167">167</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1988</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: GAL4, a protein that activates transcription in yeast, is shown to activate the mouse mammary tumor virus promoter in mammalian cells. Activation depends upon a GAL4-binding sequence inserted upstream of the gene. Deletion mutants of GAL4 bearing one or both of the “activating regions” required for activation in yeast also activate transcription in mammalian cells. A derivative of GAL4 that binds to DNA but cannot activate transcription in yeast also fails to activate transcription in mammalian cells. We also show that GAL4 and the glucocorticoid receptor activate the mouse mammary tumor virus promoter synergistically.</p></abstract></profileDesc><revisionDesc><change when="1987-12-11">Modified</change><change when="1988">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-NPHVWCR4-D/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>CELL</jid><aid>88905041</aid><ce:pii>0092-8674(88)90504-1</ce:pii><ce:doi>10.1016/0092-8674(88)90504-1</ce:doi><ce:copyright type="unknown" year="1988"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Article</ce:textfn></ce:dochead><ce:title>GAL4 activates gene expression in mammalian cells</ce:title><ce:author-group><ce:author><ce:given-name>Hitoshi</ce:given-name><ce:surname>Kakidani</ce:surname><ce:cross-ref refid="FN1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Mark</ce:given-name><ce:surname>Ptashne</ce:surname></ce:author><ce:affiliation><ce:textfn>Department of Biochemistry and Molecular Biology Harvard University Cambridge, Massachusetts 02138 USA</ce:textfn></ce:affiliation><ce:footnote id="FN1"><ce:label>∗</ce:label><ce:note-para>Present address: Biotechnology Research Laboratory, Tosoh Corporation, 2743-1 Hayakawa, Ayase, Kanagawa, Japan.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="25" month="11" year="1987"></ce:date-received><ce:date-revised day="11" month="12" year="1987"></ce:date-revised><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>GAL4, a protein that activates transcription in yeast, is shown to activate the mouse mammary tumor virus promoter in mammalian cells. Activation depends upon a GAL4-binding sequence inserted upstream of the gene. Deletion mutants of GAL4 bearing one or both of the “activating regions” required for activation in yeast also activate transcription in mammalian cells. A derivative of GAL4 that binds to DNA but cannot activate transcription in yeast also fails to activate transcription in mammalian cells. We also show that GAL4 and the glucocorticoid receptor activate the mouse mammary tumor virus promoter synergistically.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>GAL4 activates gene expression in mammalian cells</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>GAL4 activates gene expression in mammalian cells</title></titleInfo><name type="personal"><namePart type="given">Hitoshi</namePart><namePart type="family">Kakidani</namePart><affiliation>Department of Biochemistry and Molecular Biology Harvard University Cambridge, Massachusetts 02138 USA</affiliation><description>Present address: Biotechnology Research Laboratory, Tosoh Corporation, 2743-1 Hayakawa, Ayase, Kanagawa, Japan.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mark</namePart><namePart type="family">Ptashne</namePart><affiliation>Department of Biochemistry and Molecular Biology Harvard University Cambridge, Massachusetts 02138 USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1988</dateIssued><dateModified encoding="w3cdtf">1987-12-11</dateModified><copyrightDate encoding="w3cdtf">1988</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: GAL4, a protein that activates transcription in yeast, is shown to activate the mouse mammary tumor virus promoter in mammalian cells. Activation depends upon a GAL4-binding sequence inserted upstream of the gene. Deletion mutants of GAL4 bearing one or both of the “activating regions” required for activation in yeast also activate transcription in mammalian cells. A derivative of GAL4 that binds to DNA but cannot activate transcription in yeast also fails to activate transcription in mammalian cells. 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