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©The Author(s) 2025.
World J Hepatol. Feb 27, 2025; 17(2): 99292
Published online Feb 27, 2025. doi: 10.4254/wjh.v17.i2.99292
Published online Feb 27, 2025. doi: 10.4254/wjh.v17.i2.99292
Figure 2 Hepatitis B virus-miR-3 inhibits cGAS protein expression by binding cGAS 3'-untranslated region binding.
A: Schematic of the fluorescent reporter construct designed for the study; B: Relative luciferase activity in HepG2 cells transfected with pmirGLO cGAS wild-type or mutant fluorescent plasmids, and HBV-miR-3 agomir; C: Gradual decline in luciferase activity induced by HBV-miR-3 agomir after 72 hours; D: Dose-dependent repression of cGAS protein mediated by hepatitis B virus-miR-3 agomir after 72 hours. Each experiment was repeated three times. Data are presented as mean ± SD. P < 0.01. WT: Wild-type; MUT: Mutant; NC: Negative control.
- Citation: Xu ZY, Gao JS, He Y, Xiao XQ, Gong GZ, Zhang M. Hepatitis B virus confers innate immunity evasion through hepatitis B virus-miR-3 down-regulation of cGAS-Sting-IFN signaling. World J Hepatol 2025; 17(2): 99292
- URL: https://www.wjgnet.com/1948-5182/full/v17/i2/99292.htm
- DOI: https://dx.doi.org/10.4254/wjh.v17.i2.99292