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. 2012 Oct 2;40(22):11363–11379. doi: 10.1093/nar/gks868

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© The Author(s) 2012. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 8. — Model: mechanisms of SPOC1-associated chromatin compaction and modulation of DDR at DSBs. The interaction of SPOC1 with heterochromatin building factors KAP-1, HP1 and H3K9 KMTs and its binding to chromatin via H3K4me2/3 and/or other factors can induce chromatin compaction. DNA damage-induced DSBs in heterochromatin activate ATM kinase. This results in pan-nuclear KAP-1S824 phosphorylation and concomitant ATM recruitment to repair foci, and also to increasing accumulation at repair foci. SPOC1 is also ATM-dependently recruited to DSBs and accumulates detectably only at heterochromatic repair foci after γ-H2AX expansion and 53BP1 accumulation. The KAP-1S824 phosphorylation required for chromatin relaxation at DSBs in heterochromatin and for DNA repair is regulated by SPOC1. For more details see text.