Fig. 6
From: A positive-feedback loop between HBx and ALKBH5 promotes hepatocellular carcinogenesis
ALKBH5 favors HBx mRNA stability by regulating its m6A modification. A Map of m6A modification sites in the HBV ayw genome by MeRIP-seq of polyA-RNA isolated from HepG2.2.15 cells. Read coverage, normalized to the total number of reads mapping to the viral genome, is in green for MeRIP-seq and in yellow for input RNA-seq. The major m6A peak on HBV genome in the red box. B MeRIP-qPCR analysis of HBx mRNA, compared to the positive control. C MeRIP-qPCR analysis of HBx 3’UTR WT and MT mRNA. D RNA decay assay to detect the half-life of HBx 3’UTR WT and MT mRNA. HepG2 cells were transfected with HBx 3’UTR WT or MT plasmids and RT-qPCR was performed after actinomycin D was added. E MeRIP-qPCR analysis of HBx mRNA after silencing of ALKBH5. F Western blot analysis of HBx, WDR5 and H3K4me3 protein after silencing of ALKBH5. G Cartoon illustration of the positive feedback loop of HBx-ALKBH5.WT, widetype; MT, mutant