{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T01:35:40Z","timestamp":1791423340723,"version":"4.3.3"},"reference-count":29,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"6180","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[2014,4,11]]},"abstract":"<jats:title>Shutting Down Repair to Protect<\/jats:title>\n                  <jats:p>\n                    Cells repair DNA double-strand breaks (DSBs) by halting the cell cycle and activating the machinery involved in mending the breaks. However, during mitosis neither the DNA damage checkpoint nor DSB repair occur, apparently leaving the cell extremely vulnerable to DSBs.\n                    <jats:bold>\n                      Orthwein\n                      <jats:italic>et al.<\/jats:italic>\n                    <\/jats:bold>\n                    (p.\n                    <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" issue=\"6180\" page=\"189\" related-article-type=\"in-this-issue\" vol=\"344\" xlink:href=\"10.1126\/science.1248024\">189<\/jats:related-article>\n                    , published online 20 March) found that the DSB response was blocked by the phosphorylation of two crucial repair factors, RNF8 and PB531, preventing their recruitment to the site of damage. Restoring DSB repair during mitosis caused end-to-end chromosome fusions, which are catastrophic for chromosome segregation and normal cell division, explaining why the repair machinery is shut down during cell division.\n                  <\/jats:p>","DOI":"10.1126\/science.1248024","type":"journal-article","created":{"date-parts":[[2014,3,21]],"date-time":"2014-03-21T00:40:07Z","timestamp":1395362407000},"page":"189-193","source":"Crossref","is-referenced-by-count":329,"title":["Mitosis Inhibits DNA Double-Strand Break Repair to Guard Against Telomere Fusions"],"prefix":"10.1126","volume":"344","author":[{"given":"Alexandre","family":"Orthwein","sequence":"first","affiliation":[{"name":"The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Am\u00e9lie","family":"Fradet-Turcotte","sequence":"additional","affiliation":[{"name":"The Lunenfeld-Tanenbaum 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