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. 2016 Jan 8;14:6. doi: 10.1186/s12967-015-0752-1

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© Unger et al. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 8 — Changes in isoform phosphorylation of the target signaling protein, MEK1/2, in response to ischemia. An overview of ischemia-dependent regulation of isoforms of MEK1/2 in normal tissue of all patients analyzed is shown in a. Corresponding data for tumor tissue are shown in b. Results were displayed as fold changes normalized to sample NC5/N0 and in tumor tissue to sample NC5/T0. Kruskal–Wallis test and Dunn test for multiple comparisons were used for statistical analysis. N normal tissue, T tumor tissue, 0 before surgery, 10, 20, 45 10, 20, 45 min after resection; time points (10, 20, 45) are compared to time point 0; ^a p ≤ 0.05; ^b p ≤ 0.01; ^c p ≤ 0.001