Figure 2.
Treatment with FHD-286 depletes BRG1 occupancy on chromatin while increasing H3K27Ac occupancy on loci involved in differentiation and loss of cell viability. (A) MOLM13 cells were treated with 100 nM of FHD-286 for 16 hours. ChIP-Seq analysis was conducted with anti-BRG1 antibody. Panel shows the genome-wide peak profile and heat map of BRG1 binding at peak center ± 5 kb resolution. (B) Transcription factor binding motifs in loci with reduced BRG1 occupancy. The motif name, canonical binding motif, and the P value are shown. (C) Log2 fold decline of BRG1 binding at selected AML relevant loci in MOLM13 treated with 100 nM of FHD-286 for 16 hours. (D-E) MOLM13 cells were treated with 100 nM of FHD-286 for 16 hours. ChIP-Seq analysis was conducted with anti-H3K27Ac antibody and ranked ordering of superenhancer (ROSE) analysis was performed. (F) MOLM13 cells were treated with 100 nM of FHD-286 for 16 hours. ChIP-Seq analysis was conducted with anti-H3K27Ac antibody. Panel shows the log2 fold-increase in H3K27Ac occupancy on loci involved in differentiation and loss of viability in MOLM13 cells.

Treatment with FHD-286 depletes BRG1 occupancy on chromatin while increasing H3K27Ac occupancy on loci involved in differentiation and loss of cell viability. (A) MOLM13 cells were treated with 100 nM of FHD-286 for 16 hours. ChIP-Seq analysis was conducted with anti-BRG1 antibody. Panel shows the genome-wide peak profile and heat map of BRG1 binding at peak center ± 5 kb resolution. (B) Transcription factor binding motifs in loci with reduced BRG1 occupancy. The motif name, canonical binding motif, and the P value are shown. (C) Log2 fold decline of BRG1 binding at selected AML relevant loci in MOLM13 treated with 100 nM of FHD-286 for 16 hours. (D-E) MOLM13 cells were treated with 100 nM of FHD-286 for 16 hours. ChIP-Seq analysis was conducted with anti-H3K27Ac antibody and ranked ordering of superenhancer (ROSE) analysis was performed. (F) MOLM13 cells were treated with 100 nM of FHD-286 for 16 hours. ChIP-Seq analysis was conducted with anti-H3K27Ac antibody. Panel shows the log2 fold-increase in H3K27Ac occupancy on loci involved in differentiation and loss of viability in MOLM13 cells.

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