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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Alternative Cyclin D1 Splice Forms Differentially Regulate the DNA Damage Response</title><author><name sortKey="Li, Zhiping" sort="Li, Zhiping" uniqKey="Li Z" first="Zhiping" last="Li">Zhiping Li</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author><author><name sortKey="Jiao, Xuanmao" sort="Jiao, Xuanmao" uniqKey="Jiao X" first="Xuanmao" last="Jiao">Xuanmao Jiao</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author><author><name sortKey="Wang, Chenguang" sort="Wang, Chenguang" uniqKey="Wang C" first="Chenguang" last="Wang">Chenguang Wang</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author><author><name sortKey="Shirley, L Andrew" sort="Shirley, L Andrew" uniqKey="Shirley L" first="L. Andrew" last="Shirley">L. Andrew Shirley</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author><author><name sortKey="Elsaleh, Hany" sort="Elsaleh, Hany" uniqKey="Elsaleh H" first="Hany" last="Elsaleh">Hany Elsaleh</name><affiliation><nlm:aff id="A2"> The Australian National University, ANU College of Medicine and Health Sciences, Radiation Oncology, The Canberra Hospital, PO Box 11, Woden ACT 2606, Australia</nlm:aff></affiliation></author><author><name sortKey="Dahl, Olav" sort="Dahl, Olav" uniqKey="Dahl O" first="Olav" last="Dahl">Olav Dahl</name><affiliation><nlm:aff id="A3"> Department of Oncology, Haukeland University Hospital, N-5021, Bergen, Norway</nlm:aff></affiliation></author><author><name sortKey="Wang, Min" sort="Wang, Min" uniqKey="Wang M" first="Min" last="Wang">Min Wang</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author><author><name sortKey="Soutoglou, Evi" sort="Soutoglou, Evi" uniqKey="Soutoglou E" first="Evi" last="Soutoglou">Evi Soutoglou</name><affiliation><nlm:aff id="A4"> Cancer Department, IGBMC. 1 Rue Laurent Fries, 67404, Illkirch, France</nlm:aff></affiliation></author><author><name sortKey="Knudsen, Erik S" sort="Knudsen, Erik S" uniqKey="Knudsen E" first="Erik S." last="Knudsen">Erik S. Knudsen</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author><author><name sortKey="Pestell, Richard G" sort="Pestell, Richard G" uniqKey="Pestell R" first="Richard G." last="Pestell">Richard G. Pestell</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">20940395</idno><idno type="pmc">2970762</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2970762</idno><idno type="RBID">PMC:2970762</idno><idno type="doi">10.1158/0008-5472.CAN-10-0312</idno><date when="2010">2010</date><idno type="wicri:Area/Pmc/Corpus">001447</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001447</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Alternative Cyclin D1 Splice Forms Differentially Regulate the DNA Damage Response</title><author><name sortKey="Li, Zhiping" sort="Li, Zhiping" uniqKey="Li Z" first="Zhiping" last="Li">Zhiping Li</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author><author><name sortKey="Jiao, Xuanmao" sort="Jiao, Xuanmao" uniqKey="Jiao X" first="Xuanmao" last="Jiao">Xuanmao Jiao</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author><author><name sortKey="Wang, Chenguang" sort="Wang, Chenguang" uniqKey="Wang C" first="Chenguang" last="Wang">Chenguang Wang</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author><author><name sortKey="Shirley, L Andrew" sort="Shirley, L Andrew" uniqKey="Shirley L" first="L. Andrew" last="Shirley">L. Andrew Shirley</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author><author><name sortKey="Elsaleh, Hany" sort="Elsaleh, Hany" uniqKey="Elsaleh H" first="Hany" last="Elsaleh">Hany Elsaleh</name><affiliation><nlm:aff id="A2"> The Australian National University, ANU College of Medicine and Health Sciences, Radiation Oncology, The Canberra Hospital, PO Box 11, Woden ACT 2606, Australia</nlm:aff></affiliation></author><author><name sortKey="Dahl, Olav" sort="Dahl, Olav" uniqKey="Dahl O" first="Olav" last="Dahl">Olav Dahl</name><affiliation><nlm:aff id="A3"> Department of Oncology, Haukeland University Hospital, N-5021, Bergen, Norway</nlm:aff></affiliation></author><author><name sortKey="Wang, Min" sort="Wang, Min" uniqKey="Wang M" first="Min" last="Wang">Min Wang</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author><author><name sortKey="Soutoglou, Evi" sort="Soutoglou, Evi" uniqKey="Soutoglou E" first="Evi" last="Soutoglou">Evi Soutoglou</name><affiliation><nlm:aff id="A4"> Cancer Department, IGBMC. 1 Rue Laurent Fries, 67404, Illkirch, France</nlm:aff></affiliation></author><author><name sortKey="Knudsen, Erik S" sort="Knudsen, Erik S" uniqKey="Knudsen E" first="Erik S." last="Knudsen">Erik S. Knudsen</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author><author><name sortKey="Pestell, Richard G" sort="Pestell, Richard G" uniqKey="Pestell R" first="Richard G." last="Pestell">Richard G. Pestell</name><affiliation><nlm:aff id="A1"> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</nlm:aff></affiliation></author></analytic><series><title level="j">Cancer research</title><idno type="ISSN">0008-5472</idno><idno type="eISSN">1538-7445</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">The DNA damage response (DDR) activates downstream pathways including cell cycle checkpoints. The <italic>cyclin D1</italic> gene is overexpressed or amplified in many human cancers and is required for gastrointestinal, breast, and skin tumors in murine models. A common polymorphism in the human <italic>cyclin D1</italic> gene is alternatively spliced, resulting in cyclin D1a and D1b proteins that differ in their carboxyl terminus. Cyclin D1 overexpression enhances DNA-damage induced apoptosis. The role of cyclin D1 and the alternative splice form in regulating the DDR is not well understood. Herein cyclin D1a overexpression enhanced the DDR as characterized by induction of γH2AX phosphorylation, the assembly of DNA repair foci, and specific recruitment of DNA repair factors to chromatin, and G<sub>2</sub>/M arrest. Cyclin D1 deletion in fibroblasts or siRNA mediated reduction of endogenous cyclin D1 in colon cancer cells reduced the 5-FU-mediated DDR. Mechanistic studies demonstrated cyclin D1a, like DNA repair factors, elicited the DDR when stably associated with chromatin.</p></div></front></TEI><pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">2984705R</journal-id><journal-id journal-id-type="pubmed-jr-id">2786</journal-id><journal-id journal-id-type="nlm-ta">Cancer Res</journal-id><journal-title>Cancer research</journal-title><issn pub-type="ppub">0008-5472</issn><issn pub-type="epub">1538-7445</issn></journal-meta><article-meta><article-id pub-id-type="pmid">20940395</article-id><article-id pub-id-type="pmc">2970762</article-id><article-id pub-id-type="doi">10.1158/0008-5472.CAN-10-0312</article-id><article-id pub-id-type="manuscript">NIHMS234114</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Alternative Cyclin D1 Splice Forms Differentially Regulate the DNA Damage Response</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Li</surname><given-names>Zhiping</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Jiao</surname><given-names>Xuanmao</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Chenguang</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Shirley</surname><given-names>L. Andrew</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Elsaleh</surname><given-names>Hany</given-names></name><xref rid="A2" ref-type="aff">2</xref></contrib><contrib contrib-type="author"><name><surname>Dahl</surname><given-names>Olav</given-names></name><xref rid="A3" ref-type="aff">3</xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Min</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Soutoglou</surname><given-names>Evi</given-names></name><xref rid="A4" ref-type="aff">4</xref></contrib><contrib contrib-type="author"><name><surname>Knudsen</surname><given-names>Erik S.</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Pestell</surname><given-names>Richard G.</given-names></name><xref rid="A1" ref-type="aff">1</xref><xref rid="FN1" ref-type="author-notes">*</xref></contrib></contrib-group><aff id="A1"><label>1</label> Departments of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107</aff><aff id="A2"><label>2</label> The Australian National University, ANU College of Medicine and Health Sciences, Radiation Oncology, The Canberra Hospital, PO Box 11, Woden ACT 2606, Australia</aff><aff id="A3"><label>3</label> Department of Oncology, Haukeland University Hospital, N-5021, Bergen, Norway</aff><aff id="A4"><label>4</label> Cancer Department, IGBMC. 1 Rue Laurent Fries, 67404, Illkirch, France</aff><author-notes><corresp id="FN1"><label>*</label>Corresponding Author: Richard G. Pestell, The Kimmel Cancer Center, Department of Cancer Biology, Thomas Jefferson University, 233 South 10<sup>th</sup> Street, Philadelphia, PA 19107, Tel: 215-503-5692; Fax: 215-503-9334 For Reprints: <email>richard.pestell@jefferson.edu</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>10</day><month>9</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>12</day><month>10</month><year>2010</year></pub-date><pub-date pub-type="ppub"><day>1</day><month>11</month><year>2010</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>11</month><year>2011</year></pub-date><volume>70</volume><issue>21</issue><fpage>8802</fpage><lpage>8811</lpage><abstract><p id="P1">The DNA damage response (DDR) activates downstream pathways including cell cycle checkpoints. The <italic>cyclin D1</italic> gene is overexpressed or amplified in many human cancers and is required for gastrointestinal, breast, and skin tumors in murine models. A common polymorphism in the human <italic>cyclin D1</italic> gene is alternatively spliced, resulting in cyclin D1a and D1b proteins that differ in their carboxyl terminus. Cyclin D1 overexpression enhances DNA-damage induced apoptosis. The role of cyclin D1 and the alternative splice form in regulating the DDR is not well understood. Herein cyclin D1a overexpression enhanced the DDR as characterized by induction of γH2AX phosphorylation, the assembly of DNA repair foci, and specific recruitment of DNA repair factors to chromatin, and G<sub>2</sub>/M arrest. Cyclin D1 deletion in fibroblasts or siRNA mediated reduction of endogenous cyclin D1 in colon cancer cells reduced the 5-FU-mediated DDR. Mechanistic studies demonstrated cyclin D1a, like DNA repair factors, elicited the DDR when stably associated with chromatin.</p></abstract><contract-num rid="CA1">R01 CA132115-02
||CA</contract-num><contract-num rid="CA1">R01 CA107382-06
||CA</contract-num><contract-num rid="CA1">R01 CA086072-09
||CA</contract-num><contract-num rid="CA1">R01 CA075503-14
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||CA</contract-num><contract-sponsor id="CA1">National Cancer Institute : NCI</contract-sponsor></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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