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. 2021 Mar 19;4:363. doi: 10.1038/s42003-021-01884-x

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© The Author(s) 2021

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. 2 — a Extent of conservation in the ATM and ATR residues mutated in the indicated cancer type. “Total”: the total number of ATM or ATR residues mutated in the indicated cancer type (Supplementary Data 1 and 2). “Cons”: the number of mutated residues that are conserved in yeast Mec1 and/or Tel1 (Supplementary Data 3 and 4). “%”: the fraction of conserved residues. b Location of the conserved ATM residues mutated in the indicated cancer type (Supplementary Data 3). The human ATM polypeptide comprises 49 HEAT units and a kinase domain. “HEAT/KD”: the number of residues in the respective regions. Overall, 42% (139/336) of the conserved residues mutated in cancer are in the kinase domain. c Extent of overlap among the conserved ATM and ATR residues mutated in the indicated cancer type (Supplementary Data 3 and 4).