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. 2022 Jun 18;11(1):33. doi: 10.1038/s41389-022-00410-w

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — A, B Clonogenic survival experiments showing that, unlike TIP60 depletion, knockdown of ATM does not promote olaparib (A) or cisplatin (B) resistance of HeLa-BRCA2^KO cells. The average of three experiments, with standard deviations indicated as error bars, is shown. Asterisks indicate statistical significance (2-way ANOVA). C, D CellTiterGlo cellular proliferation experiments showing that ATM depletion increases olaparib (C) and cisplatin (D) sensitivity of HeLa-BRCA2^KO cells. The average of three experiments, with standard deviations indicated as error bars, is shown. Asterisks indicate statistical significance (2-way ANOVA). E, F CellTiterGlo cellular proliferation experiments showing that ATM inhibition by KU55933 and AZD1390 increases olaparib (E) and cisplatin (F) sensitivity of HeLa-BRCA2^KO cells. The average of three experiments, with standard deviations indicated as error bars, is shown. Asterisks indicate statistical significance (t-test, two-tailed, unpaired).