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. 2023 Mar 21;51(10):4867–4880. doi: 10.1093/nar/gkad203

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© The Author(s) 2023. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 3. — L1s had aberrant histone modifications in EBVaGC. (A) Average tag density plots showing H3K9me3 and H3K27me3 log₂FC enrichment at L1 regions in MKN7_EBVi cells compared with MKN7 cells (MKN7, green; MKN7_EBVi, red; H3K9me3, up; H3K27me3, down; FL-L1, left; non-FL-L1, right). (B) Heatmaps (down) and average tag density plots (up) showing H3K9me3, H3K27ac, H3K4me1 and H3K4me3 log₂FC enrichment at FL-L1 (MKN7_EBVi versus MKN7). Black horizon represents the missing signal in the sequencing data. (C) IGV tracks: H3K9me3, H3K4me1, H3K4me3 and H3K27ac signals of three FL-L1P members in MKN7 and MKN7_EBVi cells are shown. The represented signals were normalized by FPKM. Chr, chromosome. (D) The dot plot showing the relationship between log₂FC of the FL-L1 transcription level and the FL-L1 H3K9me3 modification level (MKN7_EBVi versus MKN7). Left panel, entire population of FL-L1; right panel, subpopulation analysis.