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. 2020 Sep 5;48(17):9710–9723. doi: 10.1093/nar/gkaa723

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© The Author(s) 2020. 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 Non-Commercial License (http://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 4. — At seDSBs, ATM prevents DNA ends merging and repair engagement to toxic NHEJ. (A–E) Immunoblotting of extracts from NALM6 (LIG4^+/+) and N114 (LIG4^−/−) cells (A), NALM6 cells (B), HCT116 (XLF^+/+) or (XLF^−/−) cells (C), U2OS cells (D), or GM00637 (control) or GM05849 (ATM-defective) human fibroblasts (E), pre-treated or not with the indicated kinase inhibitors for 1 h (10 μM ATMi, 3 μM DNA-PKi) and treated or not with 1 μM CPT for 1 h. (F) Survival to CPT of N114 LIG4 KO cells and derivatives expressing WT or ligase-dead LIG4, in the presence of 10 μM ATMi. y axis is log scale. Error bars represent s.d., Significant P-values were calculated using t-test (** P < 0.01; *** P < 0.005; **** P<0.001).