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. Author manuscript; available in PMC: 2017 Oct 13.
Published in final edited form as: Trends Cell Biol. 2010 May 3;20(7):402–409. doi: 10.1016/j.tcb.2010.04.002

Figure 1.

Figure 1

Overview of the role of CtIP in the cellular response to DSB damage. DSB damage induces checkpoint activation at the G1/S transition, within the S phase, or at the G2/M phase transition. The G1/S and G2/M checkpoints block entry to the S and M phases, respectively, whereas the intra-S phase checkpoint inhibits late origin firing and slows down DNA replication elongation. CtIP is required for activation of the G2/M checkpoint and could also act in the intra-S phase checkpoint. The phase of the cell cycle in which DSB damage occurs influences the choice of repair pathway. In the G1 phase, DNA DSBs are primarily repaired by NHEJ. In the S phase and G2 phases, DSBs can be repaired by HR as well as by NHEJ. The HR pathway requires CtIP, together with CDK, BRCA1, ATM and MRN, to initiate DSB end resection. CtIP is also involved in MMEJ, a form of NHEJ that involves limited DSB end resection.