Figure 1.

Overview of ERα-interaction sites. (A) ERα-binding sites at the TFF1 and GREB1 loci. The maximum number of overlapping tags, that is peak height is shown. Clear ERα peaks are detected in the promoter and enhancer region of the TFF1 and GREB1 gene on E2 treatment, whereas residual binding is observed in the absence of ligand. ERα binding is strongly decreased although not completely abolished on treatment with tamoxifen or fulvestrant compared with E2. (B) Genomic location of ERα-interaction sites. The majority of sites (41%) are located within an intron or distal from a gene (23%); 7% is located in promoter regions. (C) Comparison of large-scale ChIP profiling data. Venn diagram of the overlap of ERα-binding sites as identified in this study or reported by Lin et al and Lupien et al. 3305 and 1089 of the ChIP-Seq interaction sites are overlapping with the Lupien et al and Lin et al analysis (57 and 88%, respectively). (D) Venn diagram of the overlap between ERα-binding sites induced on E2, tamoxifen and fulvestrant treatment. The E2 and tamoxifen profile overlap to a large extent, but also contain preferential binding sites. Fulvestrant-liganded ERα interacts with a small number of sites that largely overlap with those found on E2 or tamoxifen induction.