Fig. 2
From: Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells

Evaluate CTCF’s DNA binding affinity by HA-ChIP-seq against ectopically expressed HA-tagged CTCF in CTCF RNA binding region deficient cells and cells depleted for global RNAs. A Schematic diagram illustrating how the HA-CTCF-ChIP-seq works in combination with triptolide and RNase A treatment. B Genomic heatmap of reproducible CTCF peaks from HA-ChIP of HA-tagged CTCF from CTCFAID2/WT cells treated with DMSO, triptolide, and RNase A. HA-CTCF-WT and HA-CTCF-dRBR ChIP-seq tracks were adapted from a previous study (GSE205218). C Summary of differential peaks by paired analysis. Up and down peaks were defined by comparing treatment groups vs DMSO, or dRBR vs WT at the cutoff of FC > 2 and P value < 0.05. Overlapped peaks were connected by the solid line. D ChIP-seq tracks from triptolide, RNase A, DMSO at the MYC locus show consistent CTCF binding across all samples (three replicates for each treatment). CTCF ChIP-seq was conducted in the same cells to compare with the HA-ChIP-seq (two replicates for each treatment). E ChIP-seq tracks from triptolide, RNase A, DMSO at the RIPOR1 locus show consistent CTCF binding across all samples. CTCF ChIP-seq was conducted in the same cells to compare with the HA-ChIP-seq (two replicates for each treatment)