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. 2017 Sep 5;7:10435. doi: 10.1038/s41598-017-10756-6

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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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H3K18ac levels are reduced in patients with TOF, and H3K18ac binds to Cx43 directly. (a,b) Immunohistochemistry (IHC) image (400×) of H3K18ac in control heart tissues (n = 13) and TOF heart tissues (n = 16). (c) H3K18ac IHC scores for control and TOF tissues. (d,e) Chromatin immunoprecipitation assays were performed with an antibody against H3K18ac, IgG (negative control) or RNA Pol II (positive control). Then, 10% input DNA and immunoprecipitated DNA were assayed by PCR and quantitative real-time polymerase chain reaction with Cx43 primers targeting the H3K18ac binding site. *p < 0.05; **p < 0.001. A red line indicates a positive result.