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. 2013 Jan 22;110(7):E575–E582. doi: 10.1073/pnas.1213839110

Fig. 3.

Fig. 3.

SbRLD activates p50/c-Rel to bind with IL-10 promoter. (A) ChIP analysis of IL-10 promoter (−482/−645) with nuclear extract derived from Mϕs infected with SbSLD (AG83) or SbRLD (BHU575/BHU138) and assessed with Abs to hyperacetylated histone H3 (Ace H3), p65, p50, and c-Rel, followed by PCR amplification. Chromatin immunoprecipitated by whole-rabbit IgG and no Abs was used as a negative control, and input DNA (5%) was used as an internal control. (B) Nuclear and cytoplasmic extracts derived from Mϕs infected with either SbSLD (AG83) or SbRLD (BHU575/BHU138) were used to analyze the expression of phspho-p50 (P-p50) and c-Rel in the nuclear extract (Nu) and the expression of whole p50 and c-Rel in the cytoplasmic extract (Cyt) by Western blot analysis, where histone was used as an internal control. (C) Analysis by EMSA of NF-κB DNA binding to IL-10 promoter-specific probes containing a WT NF-κB binding site (WT-m-IL-10 probe) or mutant NF-κB binding site (Mut-m-IL-10 probe). Sb-R LD inf, SbRLD infection. (D) Characterization of DNA binding of different NF-κB complexes to WT mIL-10 probe by supershift analysis using Abs specific for the indicated NF-κB subunits. Results in A–D are representative of three independent experiments.