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. 2022 Jul 22;7:248. doi: 10.1038/s41392-022-01034-7

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© The Author(s) 2022

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. 3 — Pharmacological inhibition of EZH2 activity by GSK126 diminishes H3K27me3 and not H3K27ac protein content in human pancreatic ductal cells. a Partial histone H3 lysine map of sites for methylation and acetylation. The transcriptionally suppressive marks, H3K27me3, H3K9me3 and H3K9me2 including permissive histone marks, H3K27ac and H3K4me3 are shown. b Dose-dependent increase of GSK126 (5 or 10 µM) for 48 h attenuates H3K27me3 in human pancreatic ductal cells. Histones and their associated proteins were prepared by acid extraction. Quantification levels of H3K27me3, H3K27ac, H3K9me2, H3K9me3 and H3K4me3 were calculated and adjusted to overall histone H3 using Li-COR Odyssey. The signal ratio calculated was as follows; H3K27me3/total H3, H3K27ac/total H3, H3K9me3/total H3, H3K9me2/total H3, and H3K4me3/total H3. Vehicle control is DMSO. Ordinary one-way ANOVA was performed on Control vs GSK-126 (*P < 0.05, ****P < 0.0001 error bars are SEM, n = 3)