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. 2019 Sep 3;6:79. doi: 10.3389/fmolb.2019.00079

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Copyright © 2019 Densham and Morris.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Following a DSB 53BP1 interacts with modified histones, (H2A-K15-ubiquitin blue circles, H4K20-dimethylation, green hexagons), the 53BP1-RIF1-Shieldin (Shld1-Shld2-Shld3-Rev7-CST) complex is recruited to sites of DNA damage where it also prevents retention of BRCA1-BARD1. Shld2 binds directly to ssDNA stretches >50 nucleotides long via three OB-folds. Together the Shieldin complex recruits DNA Polα which in turn primes DNA synthesis to fill in resected DNA ends. This prevents long range resection and repair by HDR pathways and supports repair by NHEJ.