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. 2021 Jan 1;11(2):805–823. doi: 10.7150/thno.50230

Figure 2.

Figure 2

Pharmacological inhibition of protein O-GlcNAcylation promotes HBV replication. (A-C) Immunoblot of total O-GlcNAc from tetracycline-inducible HepAD38 cells treated with or without GLUT1 inhibitor WZB117 (50 μM) (A), GFPT1 inhibitor DON (30 μM) (B), or OGT inhibitor ST04 (100 μM) (C) for 72 h. DON, 6-Diazo-5-oxo-L-norleucine; ST04, ST045849. (D-F) HBV DNA was detected via Southern blotting assay in stable HBV-expressing HepAD38 cells treated as described above. rc DNA, relaxed circular DNA; ds DNA, double-stranded DNA; ss DNA, single-stranded DNA. (G-I) Quantification of HBV core DNA levels in stable HBV-expressing HepAD38 cells treated as indicated using qPCR, n = 3. (J) Immunoblot of total O-GlcNAc from tetracycline-inducible HepAD38 cells treated with or without the OGA inhibitor TMG (100 μM) for 72 h. TMG, Thiamet G. (K-L) Southern blotting analysis of HBV DNA and qPCR quantification of HBV core DNA levels in stable HBV-expressing HepAD38 cells treated as in (J), n = 3. Data are expressed as the mean ± SD. P values were derived from unpaired, two-tailed Student's t-test in G-I and L; (*P < 0.05,**P < 0.01,***P < 0.001).