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. 2023 Sep 11;20:208. doi: 10.1186/s12974-023-02879-7

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© The Author(s) 2023

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 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. 6 — Analysis of the transcriptional consequences of H3K18la in Senescent BV2 Cells. A Heat map displaying the binding density of H3K18la with different H3K18la binding peaks in Dox-BV2 and NC-BV2, ordered by signal strength. B Genome-wide distribution of upregulated H3K18la-binding peaks in Dox-BV2. C KEGG analysis of enhanced H3K18la binding peaks at candidate target genes. D Genome browser tracks of H3K18la binding peaks at the representative target gene loci. The red rectangles indicate the peak regions of H3K18la on Nfkb1or Rela promoters. E Chip-qpcr analysis of the indicated promoter’s regions of Nfkb1 and Rela was performed using antibodies against H3K18la in Dox-BV2 and NC-BV2. Each bar represents the mean ± s.d. for triplicate experiments, *p < 0.05, **p < 0.01, ***p < 0.001, N.S.: no significance