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. 2014 Nov 5;105(12):1519–1525. doi: 10.1111/cas.12551

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© 2014 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Fig. 4 — DNA damage response in mitosis. (a) Double-strand break (DSB) induces histone H2AX phosphorylation (γH2AX) by ATM. (b) CDK1 and PLK1 phosphorylate RNF8 and 53BP1 to inhibit 53BP1 and BRCA1 localization of DSB sites. (c) CDK1 and PLK1 phosphorylate XRCC4, a regulatory subunit of the DNA ligase IV complex, to suppress canonical non-homologous end joining (C-NHEJ) activity. CtIP-dependent alternative non-homologous end joining (A-NHEJ) may prevent anaphase bridge formation.