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. 2020 Jul 31;12:116. doi: 10.1186/s13148-020-00906-5

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© The Author(s) 2020

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 — Relative abundance of differentially methylated CHTOP and INS DNA in human tissue samples by droplet dPCR. DNA from the indicated human tissues was isolated, bisulfite treated, and differentially methylated CHTOP-817, − 800, − 824, and INS DNA levels were quantitated by droplet dPCR. Data are displayed as a heatmap (blue = unmethylated, red = methylated). a Non-pancreatic tissues, each from a single donor. b Flow-sorted β cells (N = 3 donors) treated with and without proinflammatory cytokines (IL-1β and IFN-γ), α cells (N = 3 donors) treated with and without proinflammatory cytokines, and total pancreas (N = 6 donors). c Flow-sorted β cells (N = 3 donors) treated with and without proinflammatory cytokines, α cells (N = 2 donors) treated with and without proinflammatory cytokines, and total pancreas (N = 3 donors) from subjects with type 2 diabetes