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. Author manuscript; available in PMC: 2014 Dec 9.
Published in final edited form as: Cancer Cell. 2013 Dec 9;24(6):777–790. doi: 10.1016/j.ccr.2013.11.003

Figure 5. Identification of OCA-B as a DLBCL dependency by super-enhancer analysis.

Figure 5

(A) ChIP-Seq binding density for H3K27ac (blue), and BRD4 (red) at the enhancer of POU2AF1 following JQ1 (+) or vehicle (DMSO) (−) treatment. (B) ChIP-Seq reads at the POU2AF1 promoter for RNA Polymerase II (black) and H3K4me3 (green) following JQ1 (+) or vehicle (−) treatment. (C) OCA-B transcript and protein abundance in Ly1 cells treated with vehicle or 500 nM JQ1 or JQ1R (24 hr). Error bars represent SD. (D) OCA-B-target genes (leading edge, OCA-B GSEA) in Ly1 cells treated with vehicle or 500 nM JQ1 are visualized as heatmap. (E) Knockdown efficacy of two independent OCA-B shRNAs was detected by western blot (top panel). Proliferation of OCA-B-depleted cells was measured by alamar blue. The p values for control vs. each OCA-B shRNA were delineated by two-sided Student’s t-test; asterisks show p<.01. Error bars represent SD. (F–G) Knockdown efficiency of two independent shRNAs against BRD4 (F) or BRD2 (G) and the associated changes in OCA-B expression were evaluated by western blot. See also Figure S5 and Table S5.