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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">INT6/EIF3E interacts with ATM and is required for proper execution of the DNA damage response in human cells</title><author><name sortKey="Morris, Christelle" sort="Morris, Christelle" uniqKey="Morris C" first="Christelle" last="Morris">Christelle Morris</name><affiliation><nlm:aff id="A1">Unité Mixte de Recherche 5239, Centre National de la Recherche Scientifique, Ecole Normale Supérieure de Lyon, France</nlm:aff></affiliation></author><author><name sortKey="Tomimatsu, Nozomi" sort="Tomimatsu, Nozomi" uniqKey="Tomimatsu N" first="Nozomi" last="Tomimatsu">Nozomi Tomimatsu</name><affiliation><nlm:aff id="A2">Division of Molecular Radiation Biology, Department of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, USA</nlm:aff></affiliation></author><author><name sortKey="Richard, Derek J" sort="Richard, Derek J" uniqKey="Richard D" first="Derek J" last="Richard">Derek J. Richard</name><affiliation><nlm:aff id="A3">Signal Transduction Laboratory, Queensland Institute of Medical Research, Brisbane, Australia</nlm:aff></affiliation></author><author><name sortKey="Cluet, David" sort="Cluet, David" uniqKey="Cluet D" first="David" last="Cluet">David Cluet</name><affiliation><nlm:aff id="A1">Unité Mixte de Recherche 5239, Centre National de la Recherche Scientifique, Ecole Normale Supérieure de Lyon, France</nlm:aff></affiliation></author><author><name sortKey="Burma, Sandeep" sort="Burma, Sandeep" uniqKey="Burma S" first="Sandeep" last="Burma">Sandeep Burma</name><affiliation><nlm:aff id="A2">Division of Molecular Radiation Biology, Department of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, USA</nlm:aff></affiliation></author><author><name sortKey="Khanna, Kum Kum" sort="Khanna, Kum Kum" uniqKey="Khanna K" first="Kum Kum" last="Khanna">Kum Kum Khanna</name><affiliation><nlm:aff id="A3">Signal Transduction Laboratory, Queensland Institute of Medical Research, Brisbane, Australia</nlm:aff></affiliation></author><author><name sortKey="Jalinot, Pierre" sort="Jalinot, Pierre" uniqKey="Jalinot P" first="Pierre" last="Jalinot">Pierre Jalinot</name><affiliation><nlm:aff id="A1">Unité Mixte de Recherche 5239, Centre National de la Recherche Scientifique, Ecole Normale Supérieure de Lyon, France</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22508697</idno><idno type="pmc">3335344</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3335344</idno><idno type="RBID">PMC:3335344</idno><idno type="doi">10.1158/0008-5472.CAN-11-2562</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">001F10</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001F10</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">INT6/EIF3E interacts with ATM and is required for proper execution of the DNA damage response in human cells</title><author><name sortKey="Morris, Christelle" sort="Morris, Christelle" uniqKey="Morris C" first="Christelle" last="Morris">Christelle Morris</name><affiliation><nlm:aff id="A1">Unité Mixte de Recherche 5239, Centre National de la Recherche Scientifique, Ecole Normale Supérieure de Lyon, France</nlm:aff></affiliation></author><author><name sortKey="Tomimatsu, Nozomi" sort="Tomimatsu, Nozomi" uniqKey="Tomimatsu N" first="Nozomi" last="Tomimatsu">Nozomi Tomimatsu</name><affiliation><nlm:aff id="A2">Division of Molecular Radiation Biology, Department of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, USA</nlm:aff></affiliation></author><author><name sortKey="Richard, Derek J" sort="Richard, Derek J" uniqKey="Richard D" first="Derek J" last="Richard">Derek J. Richard</name><affiliation><nlm:aff id="A3">Signal Transduction Laboratory, Queensland Institute of Medical Research, Brisbane, Australia</nlm:aff></affiliation></author><author><name sortKey="Cluet, David" sort="Cluet, David" uniqKey="Cluet D" first="David" last="Cluet">David Cluet</name><affiliation><nlm:aff id="A1">Unité Mixte de Recherche 5239, Centre National de la Recherche Scientifique, Ecole Normale Supérieure de Lyon, France</nlm:aff></affiliation></author><author><name sortKey="Burma, Sandeep" sort="Burma, Sandeep" uniqKey="Burma S" first="Sandeep" last="Burma">Sandeep Burma</name><affiliation><nlm:aff id="A2">Division of Molecular Radiation Biology, Department of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, USA</nlm:aff></affiliation></author><author><name sortKey="Khanna, Kum Kum" sort="Khanna, Kum Kum" uniqKey="Khanna K" first="Kum Kum" last="Khanna">Kum Kum Khanna</name><affiliation><nlm:aff id="A3">Signal Transduction Laboratory, Queensland Institute of Medical Research, Brisbane, Australia</nlm:aff></affiliation></author><author><name sortKey="Jalinot, Pierre" sort="Jalinot, Pierre" uniqKey="Jalinot P" first="Pierre" last="Jalinot">Pierre Jalinot</name><affiliation><nlm:aff id="A1">Unité Mixte de Recherche 5239, Centre National de la Recherche Scientifique, Ecole Normale Supérieure de Lyon, France</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="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Altered expression of the <italic>INT6</italic> gene encoding the e subunit of the translational initiation factor eIF3 occurs in human breast cancers, but how INT6 relates to carcinogenesis remains unestablished. Here we show that INT6 is involved in the DNA damage response. INT6 was required for cell survival following γ-irradiation and G2/M checkpoint control. RNAi-mediated silencing of INT6 reduced phosphorylation of the checkpoint kinases CHK1 and CHK2 after DNA damage. Additionally, INT6 silencing prevented sustained accumulation of ATM at DNA damage sites in cells treated with γ-radiation or the radiomimetic drug neocarzinostatin. Mechanistically, this result could be explained by interaction of INT6 with ATM, which together with INT6 was recruited to sites of DNA damage. Lastly, INT6 silencing also reduced ubiquitylation events that promote retention of repair proteins at DNA lesions. Accordingly, accumulation of the repair factor BRCA1 was defective in the absence of INT6. Our findings reveal unexpected and striking connections of INT6 with ATM and BRCA1 and suggest that the protective action of INT6 in the onset of breast cancers relies on its involvement in the DNA damage response.</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>
<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-id journal-id-type="iso-abbrev">Cancer Res.</journal-id><journal-title-group><journal-title>Cancer Research</journal-title></journal-title-group><issn pub-type="ppub">0008-5472</issn><issn pub-type="epub">1538-7445</issn></journal-meta><article-meta><article-id pub-id-type="pmid">22508697</article-id><article-id pub-id-type="pmc">3335344</article-id><article-id pub-id-type="doi">10.1158/0008-5472.CAN-11-2562</article-id><article-id pub-id-type="manuscript">NIHMS358633</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>INT6/EIF3E interacts with ATM and is required for proper execution of the DNA damage response in human cells</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Morris</surname><given-names>Christelle</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Tomimatsu</surname><given-names>Nozomi</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Richard</surname><given-names>Derek J</given-names></name><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Cluet</surname><given-names>David</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Burma</surname><given-names>Sandeep</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Khanna</surname><given-names>Kum Kum</given-names></name><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Jalinot</surname><given-names>Pierre</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib></contrib-group><aff id="A1"><label>1</label>Unité Mixte de Recherche 5239, Centre National de la Recherche Scientifique, Ecole Normale Supérieure de Lyon, France</aff><aff id="A2"><label>2</label>Division of Molecular Radiation Biology, Department of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, USA</aff><aff id="A3"><label>3</label>Signal Transduction Laboratory, Queensland Institute of Medical Research, Brisbane, Australia</aff><author-notes><corresp id="FN1">Corresponding Author: Pierre Jalinot, Laboratoire de Biologie Moléculaire de la Cellule, Unité Mixte de Recherche 5239, Centre National de la Recherche Scientifique, Ecole Normale Supérieure de Lyon, 46 Allée d’Italie, 69364 Lyon cedex 07, France. Phone: + 33 4 7272 8563; Fax: + 33 4 7272 8080; <email>pjalinot@ens-lyon.fr</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>24</day><month>2</month><year>2012</year></pub-date><pub-date pub-type="ppub"><day>15</day><month>4</month><year>2012</year></pub-date><pub-date pub-type="pmc-release"><day>15</day><month>4</month><year>2013</year></pub-date><volume>72</volume><issue>8</issue><fpage>2006</fpage><lpage>2016</lpage><abstract><p id="P1">Altered expression of the <italic>INT6</italic> gene encoding the e subunit of the translational initiation factor eIF3 occurs in human breast cancers, but how INT6 relates to carcinogenesis remains unestablished. Here we show that INT6 is involved in the DNA damage response. INT6 was required for cell survival following γ-irradiation and G2/M checkpoint control. RNAi-mediated silencing of INT6 reduced phosphorylation of the checkpoint kinases CHK1 and CHK2 after DNA damage. Additionally, INT6 silencing prevented sustained accumulation of ATM at DNA damage sites in cells treated with γ-radiation or the radiomimetic drug neocarzinostatin. Mechanistically, this result could be explained by interaction of INT6 with ATM, which together with INT6 was recruited to sites of DNA damage. Lastly, INT6 silencing also reduced ubiquitylation events that promote retention of repair proteins at DNA lesions. Accordingly, accumulation of the repair factor BRCA1 was defective in the absence of INT6. Our findings reveal unexpected and striking connections of INT6 with ATM and BRCA1 and suggest that the protective action of INT6 in the onset of breast cancers relies on its involvement in the DNA damage response.</p></abstract><kwd-group><kwd>ATM</kwd><kwd>BRCA1</kwd><kwd>breast cancer</kwd><kwd>DNA damage</kwd><kwd>INT6-EIF3E</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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