Figure 1

Genome-wide LXR binding locations in a human macrophage-type cell line. A Overlap between LXR binding locations in T09- and vehicle-treated human macrophage-type cells (THP-1 cells treated for 3 days with 20 nM PMA) under three different stringency criteria for ChIP-Seq peak selection. The high stringency criterion is comprised of the thresholds for FDR < 1%, FE > 4 and raw P-value < 10^-10, while the two less stringent criteria were simply FDR < 1% and FDR < 5%. B De novo motif obtained using sequences for ChIP-Seq peaks with FDR < 1% (± 100 bp from peak summits) and the corresponding Transfac motif obtained from the public TOMTOM tool [25]. C Genomic region of the LXR target gene ABCA1 that is up-regulated (indicated by red color) by T09 treatment. Indicated are ChIP-Seq read alignment tracks for the IgG control (gray), the T09-treated sample (red) and the vehicle-treated sample (blue). Under each sample track the arrows indicate LXR binding locations of high stringency (red) or FDR < 1% (blue). Extra lanes indicate the location of LXR in homologous sequences of the mouse genome as previously published [18], de novo LXR binding sites within the peak area and insulator barrier regions identified via CTCF binding sites observed in CD4⁺ T cells [32].