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. 2022 Dec 7;479(23):2395–2417. doi: 10.1042/BCJ20220417

Figure 6. ChIP-QPCR analysis of EBNA2 and EBF-1 binding.

Figure 6.

(A) ChIP-QPCR for EBNA2 at the CD79B promoter in untreated EREB 2.5 cells or cells treated with β-estradiol for 4 or 8 h. Results show mean ± standard deviation from three independent ChIP experiments with percentage input signals after subtraction of IgG antibody controls expressed relative to the signal in the absence of β-estradiol at time 0. (B) ChIP-QPCR for EBNA2 binding at the EBV C promoter as in (A). (C) ChIP-QPCR for EBF-1 binding at the CD79B promoter as in (A). (D) Western blot analysis for ER-EBNA2 and endogenous EBF-1 expression in ER-EB 2.5 cells (±β-estradiol). Actin was used a loading control. (E) Representative ChIP results (from three independent experiments) for EBNA2, EBF-1 and H3acetylation at the CD79B promoter for a longer ER-EB 2.5 induction time course. Analysis as in (A). (F) Representative ChIP results (from three independent experiments) for EBNA2, EBF-1 and H3acetylation at the EBV C promoter for a longer ER-EB 2.5 induction time course.