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. 2021 Jan;31(1):131–145. doi: 10.1101/gr.262675.120

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© 2021 Tu et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genome.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 6. — Comparing MAnorm2 with other tools for group-level differential ChIP-seq analysis. (A) Differential analysis of H3K4me3 ChIP-seq data between GM12891 and GM12892. (B) Pairwise comparisons of H3K4me3 levels among GM12890, GM12891, GM12892, and SNYDER. Methods are sorted by the average true discovery proportion (among 500 top-ranked promoter intervals) across all the comparisons. (C) Differential analysis of H3K27ac ChIP-seq data between LCLs and CLL cell lines. (D) Differential analysis of Pol II ChIP-seq data between Japanese and non-Japanese LUAD cell lines. (E) Differential ATAC-seq analysis between LUAD and LUSC patients. ChIPComp is not applicable in this analysis as it requires input samples to model background noise. (F) Differential analysis of H3K36me3 ChIP-seq data between H1 and GM12891.