JunD-Menin Interaction Regulates c-Jun-mediated AP-1 Transactivation
The gene responsible for multiple endocrine neoplasia type 1, MEN1, encodes the 610-amino acid-protein, menin. Although menin has been reported to bind AP-1 transcription factor JunD and suppress its transcriptional activity, little is known about its molecular mechanisms and physiological role. To...
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| Veröffentlicht in: | ENDOCRINE JOURNAL 2004, Vol.51(3), pp.333-342 |
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| creator | IKEO, Yasuto YUMITA, Wataru SAKURAI, Akihiro HASHIZUME, Kiyoshi |
| description | The gene responsible for multiple endocrine neoplasia type 1, MEN1, encodes the 610-amino acid-protein, menin. Although menin has been reported to bind AP-1 transcription factor JunD and suppress its transcriptional activity, little is known about its molecular mechanisms and physiological role. To better understand the function of menin and its significance in tumorigenesis, we investigated the effect of wild-type and mutant menin proteins on AP-1 transactivation. In COS cells, wild-type menin suppressed JunD-mediated transactivation in a dose-dependent manner, while it augmented c-Jun-mediated transactivation also in a dose-dependent manner. These effects were lost or reduced in all menin mutants examined. Electrophoretic mobility shift assay using AP-1 binding elements as a probe revealed that menin does not affect binding of c-Jun to DNA. Coexpression of menin mutants did not affect the function of wild-type menin. Coexpression of JunD amino-terminal fragment abolished menin-mediated enhancement of c-Jun transactivation, suggesting that Menin-JunD interaction may negatively regulate the enhancing effect of menin on c-Jun-mediated transactivation in COS cells. |
| doi_str_mv | 10.1507/endocrj.51.333 |
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Although menin has been reported to bind AP-1 transcription factor JunD and suppress its transcriptional activity, little is known about its molecular mechanisms and physiological role. To better understand the function of menin and its significance in tumorigenesis, we investigated the effect of wild-type and mutant menin proteins on AP-1 transactivation. In COS cells, wild-type menin suppressed JunD-mediated transactivation in a dose-dependent manner, while it augmented c-Jun-mediated transactivation also in a dose-dependent manner. These effects were lost or reduced in all menin mutants examined. Electrophoretic mobility shift assay using AP-1 binding elements as a probe revealed that menin does not affect binding of c-Jun to DNA. Coexpression of menin mutants did not affect the function of wild-type menin. Coexpression of JunD amino-terminal fragment abolished menin-mediated enhancement of c-Jun transactivation, suggesting that Menin-JunD interaction may negatively regulate the enhancing effect of menin on c-Jun-mediated transactivation in COS cells.</description><identifier>ISSN: 0918-8959</identifier><identifier>EISSN: 1348-4540</identifier><identifier>DOI: 10.1507/endocrj.51.333</identifier><identifier>PMID: 15256779</identifier><language>eng</language><publisher>Japan: The Japan Endocrine Society</publisher><subject>Animals ; Blotting, Western ; Cercopithecus aethiops ; COS Cells ; DNA - metabolism ; Endocrine tumor ; Gene Expression ; Humans ; MEN1 gene ; Mice ; Multiple Endocrine Neoplasia Type 1 ; Mutation ; Peptide Fragments - genetics ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - pharmacology ; Proto-Oncogene Proteins - physiology ; Proto-Oncogene Proteins c-jun - genetics ; Proto-Oncogene Proteins c-jun - physiology ; Recombinant Fusion Proteins ; Signal transduction ; Transcription Factor AP-1 - physiology ; Transcriptional Activation ; Transfection ; Tumor suppressor</subject><ispartof>Endocrine Journal, 2004, Vol.51(3), pp.333-342</ispartof><rights>The Japan Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c645t-c5f8f567f57b973e36378a1588dc76829467bc6dbcd226bd00917650d7d0e7fe3</citedby><cites>FETCH-LOGICAL-c645t-c5f8f567f57b973e36378a1588dc76829467bc6dbcd226bd00917650d7d0e7fe3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1876,4009,27902,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15256779$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>IKEO, Yasuto</creatorcontrib><creatorcontrib>YUMITA, Wataru</creatorcontrib><creatorcontrib>SAKURAI, Akihiro</creatorcontrib><creatorcontrib>HASHIZUME, Kiyoshi</creatorcontrib><creatorcontrib>Division of Medical Genetics</creatorcontrib><creatorcontrib>Department of Aging Medicine and Geriatrics</creatorcontrib><creatorcontrib>Shinshu University School of Medicine</creatorcontrib><creatorcontrib>Shinshu University Graduate School of Medicine</creatorcontrib><creatorcontrib>Department of Preventive Medicine</creatorcontrib><title>JunD-Menin Interaction Regulates c-Jun-mediated AP-1 Transactivation</title><title>ENDOCRINE JOURNAL</title><addtitle>Endocr J</addtitle><description>The gene responsible for multiple endocrine neoplasia type 1, MEN1, encodes the 610-amino acid-protein, menin. Although menin has been reported to bind AP-1 transcription factor JunD and suppress its transcriptional activity, little is known about its molecular mechanisms and physiological role. To better understand the function of menin and its significance in tumorigenesis, we investigated the effect of wild-type and mutant menin proteins on AP-1 transactivation. In COS cells, wild-type menin suppressed JunD-mediated transactivation in a dose-dependent manner, while it augmented c-Jun-mediated transactivation also in a dose-dependent manner. These effects were lost or reduced in all menin mutants examined. Electrophoretic mobility shift assay using AP-1 binding elements as a probe revealed that menin does not affect binding of c-Jun to DNA. Coexpression of menin mutants did not affect the function of wild-type menin. Coexpression of JunD amino-terminal fragment abolished menin-mediated enhancement of c-Jun transactivation, suggesting that Menin-JunD interaction may negatively regulate the enhancing effect of menin on c-Jun-mediated transactivation in COS cells.</description><subject>Animals</subject><subject>Blotting, Western</subject><subject>Cercopithecus aethiops</subject><subject>COS Cells</subject><subject>DNA - metabolism</subject><subject>Endocrine tumor</subject><subject>Gene Expression</subject><subject>Humans</subject><subject>MEN1 gene</subject><subject>Mice</subject><subject>Multiple Endocrine Neoplasia Type 1</subject><subject>Mutation</subject><subject>Peptide Fragments - genetics</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - pharmacology</subject><subject>Proto-Oncogene Proteins - physiology</subject><subject>Proto-Oncogene Proteins c-jun - genetics</subject><subject>Proto-Oncogene Proteins c-jun - physiology</subject><subject>Recombinant Fusion Proteins</subject><subject>Signal transduction</subject><subject>Transcription Factor AP-1 - physiology</subject><subject>Transcriptional Activation</subject><subject>Transfection</subject><subject>Tumor suppressor</subject><issn>0918-8959</issn><issn>1348-4540</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkEtP3DAUhS1UVKa02y6rrLrz9DqOH1mi4VEqEFVF15Zj39CMMg7YCRL_HocMRWz8kD-fc88h5CuDNROgfmDwg4vbtWBrzvkBWTFeaVqJCj6QFdRMU12L-oh8SmkLwLmo-EdyxEQppFL1ipz-msIpvcbQheIyjBitG7shFH_wburtiKlwNCN0h77LV1-c_KasuI02pJl8tDP9mRy2tk_4Zb8fk7_nZ7ebn_Tq5uJyc3JFnazESJ1odZt9W6GaWnHkkittmdDaOyV1WVdSNU76xvmylI2HPL-SArzygKpFfky-L7r3cXiYMI1m1yWHfW8DDlMyUirQoEQG1wvo4pBSxNbcx25n45NhYObezL43I5jJveUP3_bKU5OjvuH7ojJwvgBzEc72Q-i7gGY7TDHkyMY9yBdJUwJUBkAw4AayW-48H3hVzmFLloU2i9A2jfYO_zvZOHaux3eDLcss8Prq_tmYEf4MESeX9A</recordid><startdate>2004</startdate><enddate>2004</enddate><creator>IKEO, Yasuto</creator><creator>YUMITA, Wataru</creator><creator>SAKURAI, Akihiro</creator><creator>HASHIZUME, Kiyoshi</creator><general>The Japan Endocrine Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>2004</creationdate><title>JunD-Menin Interaction Regulates c-Jun-mediated AP-1 Transactivation</title><author>IKEO, Yasuto ; YUMITA, Wataru ; SAKURAI, Akihiro ; HASHIZUME, Kiyoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c645t-c5f8f567f57b973e36378a1588dc76829467bc6dbcd226bd00917650d7d0e7fe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Blotting, Western</topic><topic>Cercopithecus aethiops</topic><topic>COS Cells</topic><topic>DNA - metabolism</topic><topic>Endocrine tumor</topic><topic>Gene Expression</topic><topic>Humans</topic><topic>MEN1 gene</topic><topic>Mice</topic><topic>Multiple Endocrine Neoplasia Type 1</topic><topic>Mutation</topic><topic>Peptide Fragments - genetics</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - pharmacology</topic><topic>Proto-Oncogene Proteins - physiology</topic><topic>Proto-Oncogene Proteins c-jun - genetics</topic><topic>Proto-Oncogene Proteins c-jun - physiology</topic><topic>Recombinant Fusion Proteins</topic><topic>Signal transduction</topic><topic>Transcription Factor AP-1 - physiology</topic><topic>Transcriptional Activation</topic><topic>Transfection</topic><topic>Tumor suppressor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>IKEO, Yasuto</creatorcontrib><creatorcontrib>YUMITA, Wataru</creatorcontrib><creatorcontrib>SAKURAI, Akihiro</creatorcontrib><creatorcontrib>HASHIZUME, Kiyoshi</creatorcontrib><creatorcontrib>Division of Medical Genetics</creatorcontrib><creatorcontrib>Department of Aging Medicine and Geriatrics</creatorcontrib><creatorcontrib>Shinshu University School of Medicine</creatorcontrib><creatorcontrib>Shinshu University Graduate School of Medicine</creatorcontrib><creatorcontrib>Department of Preventive Medicine</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>ENDOCRINE JOURNAL</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>IKEO, Yasuto</au><au>YUMITA, Wataru</au><au>SAKURAI, Akihiro</au><au>HASHIZUME, Kiyoshi</au><aucorp>Division of Medical Genetics</aucorp><aucorp>Department of Aging Medicine and Geriatrics</aucorp><aucorp>Shinshu University School of Medicine</aucorp><aucorp>Shinshu University Graduate School of Medicine</aucorp><aucorp>Department of Preventive Medicine</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>JunD-Menin Interaction Regulates c-Jun-mediated AP-1 Transactivation</atitle><jtitle>ENDOCRINE JOURNAL</jtitle><addtitle>Endocr J</addtitle><date>2004</date><risdate>2004</risdate><volume>51</volume><issue>3</issue><spage>333</spage><epage>342</epage><pages>333-342</pages><issn>0918-8959</issn><eissn>1348-4540</eissn><abstract>The gene responsible for multiple endocrine neoplasia type 1, MEN1, encodes the 610-amino acid-protein, menin. Although menin has been reported to bind AP-1 transcription factor JunD and suppress its transcriptional activity, little is known about its molecular mechanisms and physiological role. To better understand the function of menin and its significance in tumorigenesis, we investigated the effect of wild-type and mutant menin proteins on AP-1 transactivation. In COS cells, wild-type menin suppressed JunD-mediated transactivation in a dose-dependent manner, while it augmented c-Jun-mediated transactivation also in a dose-dependent manner. These effects were lost or reduced in all menin mutants examined. Electrophoretic mobility shift assay using AP-1 binding elements as a probe revealed that menin does not affect binding of c-Jun to DNA. Coexpression of menin mutants did not affect the function of wild-type menin. Coexpression of JunD amino-terminal fragment abolished menin-mediated enhancement of c-Jun transactivation, suggesting that Menin-JunD interaction may negatively regulate the enhancing effect of menin on c-Jun-mediated transactivation in COS cells.</abstract><cop>Japan</cop><pub>The Japan Endocrine Society</pub><pmid>15256779</pmid><doi>10.1507/endocrj.51.333</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Blotting, Western Cercopithecus aethiops COS Cells DNA - metabolism Endocrine tumor Gene Expression Humans MEN1 gene Mice Multiple Endocrine Neoplasia Type 1 Mutation Peptide Fragments - genetics Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - pharmacology Proto-Oncogene Proteins - physiology Proto-Oncogene Proteins c-jun - genetics Proto-Oncogene Proteins c-jun - physiology Recombinant Fusion Proteins Signal transduction Transcription Factor AP-1 - physiology Transcriptional Activation Transfection Tumor suppressor |
| title | JunD-Menin Interaction Regulates c-Jun-mediated AP-1 Transactivation |
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