Figure 5
Figure 5. PML-RARα and AML1-ETO binding sites share similar chromatin characteristics. (A) Percentage of PML-RARα binding sites in the different CATCH-defined enhancer clusters. Clusters 1b, 1c, and 1d from Figure 4 were examined for their relative PML-RARα presence. (B) Enrichment of the accessible regions identified in SKNO-1 cells at AML1-ETO binding sites. The plot represents the number of accessible regions enriched over a distance of ± 10 kb starting from the middle of the AML1-ETO binding sites. (C) H2A.Z acetylation and AML1-ETO tag density at p300 binding sites in SKNO-1 cells. p300 binding sites were called using MACS. (D) Overview of AML1-ETO (red), p300 (green), and H2A.Z acetylation (orange) at the PLEKHB2 and ATP2A2 genomic regions showing p300 and AML1-ETO binding but H2A.Z hypoacetylation.

PML-RARα and AML1-ETO binding sites share similar chromatin characteristics. (A) Percentage of PML-RARα binding sites in the different CATCH-defined enhancer clusters. Clusters 1b, 1c, and 1d from Figure 4 were examined for their relative PML-RARα presence. (B) Enrichment of the accessible regions identified in SKNO-1 cells at AML1-ETO binding sites. The plot represents the number of accessible regions enriched over a distance of ± 10 kb starting from the middle of the AML1-ETO binding sites. (C) H2A.Z acetylation and AML1-ETO tag density at p300 binding sites in SKNO-1 cells. p300 binding sites were called using MACS. (D) Overview of AML1-ETO (red), p300 (green), and H2A.Z acetylation (orange) at the PLEKHB2 and ATP2A2 genomic regions showing p300 and AML1-ETO binding but H2A.Z hypoacetylation.

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