Fig. 6
From: Super enhancers targeting ZBTB16 in osteogenesis protect against osteoporosis
BRD4 navigates the translocation of the RPAP2-Pol II complex to SEs and drives ZBTB16 transcription. a Co-IP experiment showing the binding of RPAP2 and RPB1. b Immunofluorescence showing the effects of RPAP2 knockdown, leptomycin B pretreatment prior to RPAP2 knockdown and JQ1 treatment on the subcellular distribution of RPAP2 and RPB1 in MSCs. c–f Western blot analysis of protein fractions showing the distribution of RPB1, BRD4 and RPAP2 in the cytoplasm, nucleus and chromatin. Tubulin, lamin A/C and histone 3 were the internal controls for proteins in the cytoplasm, nucleus and chromatin, respectively (c). Scatter plots showing the respective abundances of RPB1 (d), BRD4 (e) and RPAP2 (f) in different protein extracts. g ChIP-seq signal traces showing POL II binding to ZBTB16 in NC or OB group MSCs. h Location of ChIP‒qPCR primers for ZBTB16. i ChIP‒qPCR analysis showing POL II occupancy on ZBTB16 in NC and OB group MSCs. j ChIP‒qPCR analysis showing the effects of JQ1 treatment, leptomycin B and leptomycin B pretreatment prior to RPAP2 knockdown on POL II occupancy on ZBTB16 in MSCs. The statistical data are represented as the means ± SEMs, n = 9, *P < 0.05, **P < 0.01, ***P < 0.005, ****P < 0.001
