Figure 3.

ChIP analysis of Fli-1 binding to the CXCL10 promoter, but Fli-1 failed to drive transcription from the CXCL10 promoter. (A) Putative Fli-1 binding sites within the murine CXCL10 promoter and the location of the primers used for the ChIP assay. The number of potential binding sites for each primer set is noted above. (B) FLI-1 binding in the ChIP assay was determined by enrichment of the indicated CXCL10 regions by IP with anti-Fli-1 antibody relative to enrichment of regions by IP with a control IgG antibody. A pair of primers for the MCP1 promoter previously shown to be enriched in a ChIP assay by anti-Fli-1 antibody was used as ChIP Control. * Indicates p<0.05. Data were represented as mean ± SEM from three independent experiments. (C) Human CXCL10 promoter cloned into the pGL3 vector, upstream of the luciferase reporter gene co-transfected with increasing amounts of a Fli-1 expression vector (0.05, 0.1, 0.2, 0.25, 0.5, 1 and 2 μg). Co-transfection of a NFkBp65 expression vector (0.5µg) was used as positive control. Values shown are fold activation over the empty vector control (mean + SEM for three replicate experiments; n = 9), * Indicates p<0.05.