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. 2019 Oct 1;9:14134. doi: 10.1038/s41598-019-50785-x

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© The Author(s) 2019

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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Epigenetic regulation via acetylation by DAMTC to mitigate GI-ARS in TBI mice. Effects of DAMTC on acetylation in TBI mice by immunoblotting analysis of acetyl-Histone H3 (at lysine 9/14) in the intestinal jejunum. Changes in the protein levels of naïve, DAMTC, TBI (7.6 Gy), and TBI + DAMTC mice at days (A) 3, (B) 7 and (C) 21 following TBI. Blots represented are from the same gel and β-actin served as the loading control. Membrane stripping to re-probe for a different protein was done wherever required. Quantifical analysis of immunoblots represent average relative fold change in protein levels (normalized to β-actin) with SEM between TBI (7.6 Gy) and TBI + DAMTC cohorts (from five independent observations).