{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T19:27:09Z","timestamp":1790882829093,"version":"4.1.0"},"reference-count":41,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2018,11,6]],"date-time":"2018-11-06T00:00:00Z","timestamp":1541462400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2018,12,21]],"date-time":"2018-12-21T00:00:00Z","timestamp":1545350400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2018,12,21]]},"abstract":"<jats:p>\n            <jats:named-content content-type=\"genus-species\">Chlamydia trachomatis<\/jats:named-content>\n            induces DNA double-strand breaks in host cells but simultaneously inhibits proper DNA damage response and repair mechanisms. This may render host cells prone to loss of genetic integrity and transformation. Here we show that\n            <jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>\n            prevents activation of the key DNA damage response mediator ATM by preventing the release from PP2A, leading to a complete absence of homologous recombination repair in host cells.\n          <\/jats:p>","DOI":"10.1128\/mbio.01465-18","type":"journal-article","created":{"date-parts":[[2018,11,6]],"date-time":"2018-11-06T10:47:27Z","timestamp":1541501247000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["<i>Chlamydia trachomatis<\/i>\n            Inhibits Homologous Recombination Repair of DNA Breaks by Interfering with PP2A Signaling"],"prefix":"10.1128","volume":"9","author":[{"given":"Yang","family":"Mi","sequence":"first","affiliation":[{"name":"Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany"},{"name":"Key Laboratory of H. 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