Figure 7
The NF-κB complex directly binds to ISRE and drives its transcriptional activity.
(A) NF-κ B and ISRE sequence specific binding regions. Their consensus nucleotides are labeled in red color and the consensus region is enclosed by the rectangular box. (B) Heatmaps display the normalized ChIP-seq reads representing the binding intensity of STAT1 and RelA. Displayed are 8 kb regions centered on the summits of significant STAT1 and/or RelA binding sites. The heatmap are clustered for the STAT1 and RelA binding signal based on the central 0.5 kb of the heatmap. left) Heatmaps of all significant STAT1 and RelA binding sites (n = 13367). right) Heatmap of all significant STAT1 and RelA binding sites that are within 1 kb of a transcription start site (n = 4545). (C) Binding of RelA to the promoters of the indicated ISGs. Sequence reads from anti-RelA ChIP-seq or rabbit-IgG-control were plotted relative to chromosomal position. Genome location of corresponding ISGs is shown beneath the track signaling. RelA shows strong and specific binding on the promoters of indicated ISGs, while the rabbit-IgG, serving as negative control, shows no significant binding. (D) In the Huh7 cell-based mutant ISRE luciferase reporter cells, TNF-α did not induce mutant ISRE related luciferase activation as measured at 3 different time points (n = 3 independent experiments with 2–3 replicates each). Data presented as mean SD (*P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant).
