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Fig. 5 | Genome Medicine

Fig. 5

From: TCF21 and AP-1 interact through epigenetic modifications to regulate coronary artery disease gene expression

Fig. 5

JUN and TCF21 co-localize genome-wide and regulate H3K27ac chromatin modification. a JUN ChIPseq peaks and b TCF21 peaks were extended +/− 2 kb from summit, and a density plot created for RPM normalized enrichment levels of JUN, TCF21, and H3K27ac ChIPseq in HACSMC, along with control transcription factor HNF1A. c The number of TCF21 peaks overlapped with JUN binding for distances between peaks less than 1 kb, 5 kb, and 10 kb. d Heatmap distribution of ChIPseq data for JUN, TCF21, and H3K27ac with control (Ctrl) or JUN knockdown (JUN-KD) centered on JUN peaks, or e TCF21 knockdown (TCF21-KD) centered on TCF21 peaks within a 4-kb window. f Peak length distribution of Ctrl or JUN-KD, and g Ctrl or TCF21-KD H3K27ac ChIPseq in HCASMC (box plots with Wilcoxon tests, P < 2.2e−16). h H3K27ac ChIPseq enrichment level of Ctrl or JUN-KD, and i Ctrl or TCF21-KD, centered on all H3K27ac peaks with +/− 2 kb extension, normalized by RPM

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