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Fig. 7 | Genome Medicine

Fig. 7

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

Fig. 7

Allele-specific binding of JUN, TCF21, and H3K27ac enrichment at the SMAD3 locus. a HaploChIP of JUN, TCF21, H3K27ac, and ATAC at rs17293632 was evaluated by qPCR with allele-specific TaqMan probes in heterozygous HCASMCs. Enrichment was normalized with input, and data was shown as C/T ratio. b SMAD3 expression levels in wild type (WT), deletion (DEL), or converted (ALT) HEK293 CRISPR/Cas9 edited cell lines as detected by qPCR. The genomic sequence of CRISPR edits are shown for corresponding cell lines. c ChIP-qPCR of JUN, d TCF21, e H3K27ac, and f ATAC-qPCR showing the differential transcription factor binding, H3K27ac modification, or ATACseq open chromatin at SMAD3-1, SMAD3-2, and CDKN2BAS locus regions for WT or CRISPR HEK293 cell lines. Dominant negative A-FOS was expressed as a positive control of JUN inhibition, and all data normalized versus input (mean ± SD, n = 3)

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