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. 2021 Sep 22;49(18):10275–10288. doi: 10.1093/nar/gkab796

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© The Author(s) 2021. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 6. — (A) Double-strand breaks (DSB) and stalled replication forks are repaired by HR and NHEJ, mediated by DNA-PK and ATM kinases and RAD51. Created with BioRender. Chemical structure of DDR inhibitors NU7441 (DNA-PKi), KU55933 (ATMi) and B02 (RAD51i). (B) 3D pyramid plots showing the percentage of extra cell death for the combination of TrisNP (lethal concentration range: 0–40 μM), with DNA-PKi, ATMi, or RAD51i (non-lethal concentration range, see Supplementary Data). Results are the average of three separate experiments each containing technical duplicates. (C) Normalised isobolograms for combination of TrisPOB or TrisNP with DNA-PKi (circles), ATMi (triangles), and RAD51i (squares). Points above the grey horizontal line show antagonism between agents, below the line show synergism. Combination index graph (right) of the same co-treatments. Derived from the same raw data as the pyramid plots in Figure 5B.