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. 2020 Dec 15;40(6):1147–1161. doi: 10.1038/s41388-020-01593-5

Fig. 6. Truncated HBx downregulates the expression of TXNIP by transactivation through NFATC2.

Fig. 6

A Relative luciferase activity in each of the truncated mutants of TXNIP promoter (T1, T2, T3, and T4), the full length of TXNIP promoter (FL), and HBx containing samples indicated by dual-luciferase reporter assay. B Schematic illustrator of the luciferase reporter constructs containing different lengths of truncated mutants of TXNIP promoter. C Prediction of the cis-regulatory elements between nt-1893 and nt-1359 on the promoter of TXNIP by JASPAR revealed three NFATC2 binding sites, one MYOG binding site, one STAT3 binding site, and one FOXO1 binding site. D Relative luciferase activity after mutagenesis of the candidate binding sites indicated by dual-luciferase reporter assay, TI and T2 are served as a negative and positive control. Mutagenesis of MYOG, STAT3, and FOXO1 showed little change in the luciferase activity, and NFATC2 is essential for the transcription downregulation induced by truncated HBx. E The binding of NFATC2 to the promoter of TXNIP mediated by truncated HBx was validated by the CHIP assay.