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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">ANKRD1 Acts as a Transcriptional Repressor of <italic>MMP13</italic> via the AP-1 Site</title><author><name sortKey="Almod Var Garcia, Karinna" sort="Almod Var Garcia, Karinna" uniqKey="Almod Var Garcia K" first="Karinna" last="Almod Var-García">Karinna Almod Var-García</name><affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Kwon, Minjae" sort="Kwon, Minjae" uniqKey="Kwon M" first="Minjae" last="Kwon">Minjae Kwon</name><affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Samaras, Susan E" sort="Samaras, Susan E" uniqKey="Samaras S" first="Susan E." last="Samaras">Susan E. Samaras</name><affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Davidson, Jeffrey M" sort="Davidson, Jeffrey M" uniqKey="Davidson J" first="Jeffrey M." last="Davidson">Jeffrey M. Davidson</name><affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">VA Tennessee Valley Healthcare System, Nashville, Tennessee, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24515436</idno><idno type="pmc">3993579</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993579</idno><idno type="RBID">PMC:3993579</idno><idno type="doi">10.1128/MCB.01357-13</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">003089</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">003089</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">ANKRD1 Acts as a Transcriptional Repressor of <italic>MMP13</italic> via the AP-1 Site</title><author><name sortKey="Almod Var Garcia, Karinna" sort="Almod Var Garcia, Karinna" uniqKey="Almod Var Garcia K" first="Karinna" last="Almod Var-García">Karinna Almod Var-García</name><affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Kwon, Minjae" sort="Kwon, Minjae" uniqKey="Kwon M" first="Minjae" last="Kwon">Minjae Kwon</name><affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Samaras, Susan E" sort="Samaras, Susan E" uniqKey="Samaras S" first="Susan E." last="Samaras">Susan E. Samaras</name><affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff></affiliation></author><author><name sortKey="Davidson, Jeffrey M" sort="Davidson, Jeffrey M" uniqKey="Davidson J" first="Jeffrey M." last="Davidson">Jeffrey M. Davidson</name><affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">VA Tennessee Valley Healthcare System, Nashville, Tennessee, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Molecular and Cellular Biology</title><idno type="ISSN">0270-7306</idno><idno type="eISSN">1098-5549</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The transcriptional cofactor ANKRD1 is sharply induced during wound repair, and its overexpression enhances healing. We recently found that global deletion of murine <italic>Ankrd1</italic> impairs wound contraction and enhances necrosis of ischemic wounds. A quantitative PCR array of <italic>Ankrd1</italic><sup>−/−</sup> (KO) fibroblasts indicated that ANKRD1 regulates MMP genes. Yeast two-hybrid and coimmunoprecipitation analyses associated ANKRD1 with nucleolin, which represses AP-1 activation of <italic>MMP13. Ankrd1</italic> deletion enhanced both basal and phorbol 12-myristate 13-acetate (PMA)-induced <italic>MMP13</italic> promoter activity; conversely, <italic>Ankrd1</italic> overexpression in control cells decreased PMA-induced <italic>MMP13</italic> promoter activity. <italic>Ankrd1</italic> reconstitution in KO fibroblasts decreased <italic>MMP13</italic> mRNA, while <italic>Ankrd1</italic> knockdown increased these levels. <italic>MMP13</italic> mRNA and protein were elevated in intact skin and wounds of KO versus <italic>Ankrd1</italic><sup><italic>fl/fl</italic></sup> (FLOX) mice. Electrophoretic mobility shift assay gel shift patterns suggested that additional transcription factors bind to the <italic>MMP13</italic> AP-1 site in the absence of <italic>Ankrd1</italic>, and this concept was reinforced by chromatin immunoprecipitation analysis as greater binding of c-Jun to the AP-1 site in extracts from FLOX versus KO fibroblasts. We propose that ANKRD1, in association with factors such as nucleolin, represses <italic>MMP13</italic> transcription. <italic>Ankrd1</italic> deletion additionally relieved <italic>MMP10</italic> transcriptional repression. Nuclear ANKRD1 appears to modulate extracellular matrix remodeling by MMPs.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Mol Cell Biol</journal-id><journal-id journal-id-type="iso-abbrev">Mol. Cell. Biol</journal-id><journal-id journal-id-type="hwp">mcb</journal-id><journal-id journal-id-type="pmc">mcb</journal-id><journal-id journal-id-type="publisher-id">MCB</journal-id><journal-title-group><journal-title>Molecular and Cellular Biology</journal-title></journal-title-group><issn pub-type="ppub">0270-7306</issn><issn pub-type="epub">1098-5549</issn><publisher><publisher-name>American Society for Microbiology</publisher-name><publisher-loc>1752 N St., N.W., Washington, DC</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">24515436</article-id><article-id pub-id-type="pmc">3993579</article-id><article-id pub-id-type="publisher-id">01357-13</article-id><article-id pub-id-type="doi">10.1128/MCB.01357-13</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group></article-categories><title-group><article-title>ANKRD1 Acts as a Transcriptional Repressor of <italic>MMP13</italic> via the AP-1 Site</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Almodóvar-García</surname><given-names>Karinna</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Kwon</surname><given-names>Minjae</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Samaras</surname><given-names>Susan E.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Davidson</surname><given-names>Jeffrey M.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><aff id="aff1"><label>a</label>Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</aff><aff id="aff2"><label>b</label>VA Tennessee Valley Healthcare System, Nashville, Tennessee, USA</aff></contrib-group><author-notes><corresp id="cor1">Address correspondence to Jeffrey M. Davidson, <email>jeff.davidson@vanderbilt.edu</email>.</corresp></author-notes><pub-date pub-type="ppub"><month>4</month><year>2014</year></pub-date><volume>34</volume><issue>8</issue><fpage>1500</fpage><lpage>1511</lpage><history><date date-type="received"><day>9</day><month>10</month><year>2013</year></date><date date-type="rev-request"><day>2</day><month>12</month><year>2013</year></date><date date-type="accepted"><day>31</day><month>1</month><year>2014</year></date></history><permissions><copyright-statement>Copyright © 2014, American Society for Microbiology. All Rights Reserved.</copyright-statement><copyright-year>2014</copyright-year><copyright-holder>American Society for Microbiology</copyright-holder></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zmb00814001500.pdf"></self-uri><abstract><p>The transcriptional cofactor ANKRD1 is sharply induced during wound repair, and its overexpression enhances healing. We recently found that global deletion of murine <italic>Ankrd1</italic> impairs wound contraction and enhances necrosis of ischemic wounds. A quantitative PCR array of <italic>Ankrd1</italic><sup>−/−</sup> (KO) fibroblasts indicated that ANKRD1 regulates MMP genes. Yeast two-hybrid and coimmunoprecipitation analyses associated ANKRD1 with nucleolin, which represses AP-1 activation of <italic>MMP13. Ankrd1</italic> deletion enhanced both basal and phorbol 12-myristate 13-acetate (PMA)-induced <italic>MMP13</italic> promoter activity; conversely, <italic>Ankrd1</italic> overexpression in control cells decreased PMA-induced <italic>MMP13</italic> promoter activity. <italic>Ankrd1</italic> reconstitution in KO fibroblasts decreased <italic>MMP13</italic> mRNA, while <italic>Ankrd1</italic> knockdown increased these levels. <italic>MMP13</italic> mRNA and protein were elevated in intact skin and wounds of KO versus <italic>Ankrd1</italic><sup><italic>fl/fl</italic></sup> (FLOX) mice. Electrophoretic mobility shift assay gel shift patterns suggested that additional transcription factors bind to the <italic>MMP13</italic> AP-1 site in the absence of <italic>Ankrd1</italic>, and this concept was reinforced by chromatin immunoprecipitation analysis as greater binding of c-Jun to the AP-1 site in extracts from FLOX versus KO fibroblasts. We propose that ANKRD1, in association with factors such as nucleolin, represses <italic>MMP13</italic> transcription. <italic>Ankrd1</italic> deletion additionally relieved <italic>MMP10</italic> transcriptional repression. Nuclear ANKRD1 appears to modulate extracellular matrix remodeling by MMPs.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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