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. 2017 Sep 28;6:1779. [Version 1] doi: 10.12688/f1000research.12110.1

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Copyright: © 2017 Shamanna RA et al.

This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

The author(s) is/are employees of the US Government and therefore domestic copyright protection in USA does not apply to this work. The work may be protected under the copyright laws of other jurisdictions when used in those jurisdictions.

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Figure 1. — DSBs generated by extrinsic and intrinsic factors are recognized by the sensor proteins Ku70/Ku80, WRN, MRN, and PARP1 to mediate repair. DSBs are repaired via classical/canonical non-homologous end joining (c-NHEJ), alternative (alt)-NHEJ, and homologous recombination (HR) pathways. WRN promotes Ku-dependent c-NHEJ with its catalytic activities and strongly inhibits alt-NHEJ with its non-catalytic activities. WRN suppresses the recruitment and downstream functions of MRE11 and CtIP to inhibit alt-NHEJ. During S/G ₂ phases of the cell cycle, WRN promotes HR. Accurate repair of DSBs is required for genome stability without loss of genetic information.