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. Author manuscript; available in PMC: 2021 Oct 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2020 Aug 13;40(10):2494–2507. doi: 10.1161/ATVBAHA.120.314955

Figure 5. BAF60a is required for SWI/SNF recruitment to the promoters of NF-κB target genes.

Figure 5.

A-C and E, HASMCs were transfected with siControl or siBAF60a (30 nM). After 72 hours, ChIP-seq was performed for BRG1, H3K9Ac and H3K27Ac. A, BRG1 genomic binding on target sites within a ±2kb range centered on each peak is presented by a heatmap. B, Histogram of ChIP-seq reads of BRG1 ±3kb surrounding the TSS of NF-κB target genes. C, Normalized ChIP-seq reads of BRG1, H3K9Ac and H3K27Ac in the CXCL6 gene promoter and coding region are shown in IGV. D, BRG1 binding on the NF-κB binding site located in the mouse Cxcl6 promoter was detected by ChIP assay in primary aortic smooth muscle cells isolated from abdominal aortas of BAF60af/f and BAF60aSMKO mice. n=3. E, Normalized ChIP-seq reads of BRG1, H3K9Ac and H3K27Ac around the TSS of the CTSS gene shown in IGV. F, p65 binding on the NF-κB binding site located in the CTSS promoter was detected by ChIP assay in HASMCs transfected with 30 nM siControl or siBAF60a for 72h followed by 1h treatment with TNFα (20 ng/ml). n=3. G, Physical interaction between p300, BRG1, and BAF60a in cultured HASMCs was detected by Co-IP. IgG was used as a negative control. n=3. H, HASMCs were transfected with siControl or siBAF60a (30 nM). After 72 hours, physical interaction between p300 and BRG1 was detected by Co-IP. IgG was used as a negative control. n=3. Data are presented as mean ± SEM. Two-way-ANOVA followed by Holm-Sidak post hoc analysis for D and F.