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. 2017 Sep 11;7:11144. doi: 10.1038/s41598-017-11661-8

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© The Author(s) 2017

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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Atm-heterozygous pancreatic tumor cells activate ATM signals upon IR exposure. (A–C) Western blots show induction of phospho-Kap1 (A) and phospho-p53 (B) proteins in KC 215.2 tumor cells and KCATMΔ+ 255.9 tumors cells, 1–4 hours post-IR (4Gy). In contrast, phospho-Kap1 is largely undetected (A) and phospho-p53 is only slightly induced 24 hours post-IR (B) in KCATMΔΔ 149.4 tumor cells. (C) The expression of p21 increases in tumor cells of all 3 genotypes after exposure to 4Gy. (D) Quantitative Western blot results show similar p-Kap1/Kap1 protein ratios in KC 215.2 tumor cells and KCATMΔ+ 255.9 tumors cells, and lack of p-Kap1 induction in KCATMΔΔ 149.4 tumor cells, after 4Gy exposure. This analysis also shows very deficient phospho-p53/p53 ratio in KCATMΔΔ 149.4 irradiated cells compared to KC 215.2 and KCATMΔ+ 255.9 irradiated cells. Quantitative Western blots reveal more efficient induction of p21 in KC 215.2 cells than in KCATMΔ+ 255.9 and KCATMΔΔ 149.4 cells post-irradiation. Bars represent ± SEM values, n = 3 individual hybridizations per genotype). PT: primary tumor. LM: liver metastasis.