Fig. 7: ENBA2 promoted the acetylation of the histone H3K27 in genome-wide.

a ChIP-seq tracks of H3K27ac in the Dox-induced EBNA2+ CNE2 cells (blue track) and control CNE2 cells (purple track). b Venn diagram of H3K27ac peaks in the Dox-induced EBNA2+ CNE2 cells (green track) and control CNE2 cells (brown track), EBNA2+ BJAB cells (green track), and control cells (brown track) c Annotation of H3K27ac peaks. EBNA2+: EBNA2+ cell unique peaks, control: control cell unique peaks, common: peaks of overlapped in both cell types. d The plot and heatmap of common peaks in the Dox-induced EBNA2+ cells (blue track) and control cells (purple track), EBNA2+ BJAB cells (green track), and control cells (green track). e Selected transcription factor binding motifs overrepresented in CUT&Tag peaks, the most enriched factor for each family is shown. f Western blot of H3K27ac of the EBNA2-expressing HEK 293T cells treated with 10 μg/mL Doxycycline or vehicle for 24 h. H3 served as a loading control.