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. Author manuscript; available in PMC: 2017 Jul 1.
Published in final edited form as: Virology. 2016 Apr 26;494:158–167. doi: 10.1016/j.virol.2016.04.005

Fig. 3. Bay11 inhibits pri-miR-155 and AP1 gene expression in EBV latency type III cells.

Fig. 3

A–C. X50-7 (A) and IB4 (B & C) cells were treated with an NF-κB inhibitor and MEK kinase inhibitors for 48 hours and cells were harvested for RT-PCR to detect pri-miR-155 expression (top panel) and for western blot to detect AP1 protein expression (bottom panel). Bay-U indicates treatment with Bay 11 plus UO126. Relative expression in percentage was compared to the DMSO 2−ΔΔCT value. D. A luciferase assay was performed to analyze the activity of miR-155 promoters; wild type (155pwt) vs. AP1 mutant (155pAP1mut), in response to treatment with signaling pathway inhibitor Bay11 in IB4 cells. The relative luminescence units (RLU) fold change value is compared with the RLU measured in control (Cntl), pGL3-basic.