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. 2018 Jan 19;8:1230. doi: 10.1038/s41598-018-19370-6

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© The Author(s) 2018

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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H3K79 methylation controls antiviral response. A549 cells were plated alone or with Dot1L inhibitor (Dot1L In, 1 μM, 48 h), then left untreated (A), treated with 100 U/ml IFNαβ (B) or PR8hv-infected (1 PFU/cell) (C) during 8 or 16 h. RNA was extracted and used for qPCR detection of IFNβ, ISG56 and MX1 genes. IFNαβ treatment was used as positive control and induced a significant increase in the genes analyzed (***P < 0.001). Student’s t test with Welch’s correction; 3 technical replicates of 3 independent experiments were performed.