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. 2020 Jun 16;11:3045. doi: 10.1038/s41467-020-16853-x

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© The Author(s) 2020

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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Fig. 2 — a Mean average plot (n = 3, p < 0.05) of cellular gene expressions upon Tax. Each gene is plotted according to its expression level (log10(BaseMean) from DESeq2 analysis) and to fold change (log2-FC) upon Tax. Red dots show significant gene expression changes in HEK cells (log2-FC > 0.6, p < 0.05, Fisher’s exact test). Black dots highlight genes encoding splicing factors. DDX5 and DDX17 are indicated. b Immunoprecipitation assays (IP) were carried out in HEK cells using isotype IgG or anti-DDX17 (b, g), anti-RELA (e, g), and anti-Tax (c, g) antibodies, followed by immunoblotting (IB) with indicated antibodies. d Western blot analysis of Tax and M22 expression 48-h post-transfection. f RNA-free IP assays. g TNFa exposure of M22-expressing cells promotes RELA–DDX17 interactions. h Model of NF-κB-dependent interplay between Tax, RELA, and DDX17. For b–g, a representative image from three independent experiments is shown. Source data are provided as a Source Data file.