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. 2022 Jul 28;14:96. doi: 10.1186/s13148-022-01316-5

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 4 — Catalytic P300/CBP inhibition stymies IRF1-dependent transactivation of IFNγ-induced genes. A Column-normalized heatmap of gene expression by RNA-seq for IFNγ stimulated genes in the presence of IFNγ ± A-241. B AT3 cells stimulated with IFNγ ± A-241 for 3 h prior to immunoblot for Tubulin, STAT1, or phosphor-STAT1 (Y701). C Acetylation of H3K27 by ChIP-seq at IFNγ-induced loci following IFNγ ± A-241. D IGV screenshot of Trim21, Igtp, and Cd274 loci showing H3K27ac ChIP-Rx, ATAC-seq, and IRF1 ChIP-seq in the presence of IFNγ ± A-241. E Binding of IRF1 by ChIP-seq to IFNγ-induced loci following IFNγ ± A-241. F Chromatin accessibility by ATAC-seq at IFNγ-induced loci following IFNγ ± A-241. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001, Mann–Whitney U test