AMPK maintains histone acetylation at Brd4 binding sites. (A) Density plots of H3K9ac, H3K27ac, and H4K8ac ChIP-seq signals centered around the transcription start site. (B-C) Meta profiles of the indicated ChIP-seq dataset centered around the peak apex of 10 615 enhancer elements defined by H3K27ac signal (B) and 6522 enhancer elements defined by BRD4 occupancy based on Roe et al⁴⁶  (C). (D) A waterfall plot depicting the differences in H3K27ac signals at superenhancers between WT and AMPK KO L-GMPs. The numbers in parentheses indicate the rankings of each gene. (E) Motif analysis of H3K9ac ChIP-seq data set showing the transcription factor motifs enriched in WT L-GMPs compared with AMPK KO L-GMPs. (F) ChIP-seq occupancy profiles of H3K9ac, H3K27ac, and H4K8ac of both AMPK-proficient and AMPK-deficient L-GMPs, as well as the BRD4 profile⁴⁶  at the Myc locus. Myc enhancer elements E1-E5 are shown in pink shades. (G) ChIP-quantitative polymerase chain reaction to detect BRD4 occupancy at 2 Myc enhancers (E2 and E3) with WT and AMPK KO AML (n = 3). All data represent mean ± standard deviation. *P < .05; **P < .01; ***P < .001 by 1-way ANOVA.