Abstract：
β-catenin regulates HBV transcription in cell culture and viral biosynthesis in vivo in the transgenic mouse model of chronic HBV infection. Therefore, it is important to understand which transcription factor activities are coactivated by β-catenin to enhance HBV biosynthesis. The effect of β-catenin expression in the context of nuclear receptor-mediated HBV transcription was evaluated initially in the human embryonic kidney cell line, HEK293T. Reporter gene and viral replication assays revealed that β-catenin can coactivate HBV transcription through some, most predominantly liver receptor homolog 1 (LRH1), but not all nuclear receptors known to activate viral biosynthesis. Similarly, β-catenin activated nuclear receptor-mediated HBV transcription and replication in the human hepatoma cell line, Huh7, primarily through its effect on the farnesoid X receptor α (FXRα). These data indicate that β-catenin can enhance nuclear receptor-mediated HBV biosynthesis, but the relative importance of various transcription factors is dependent upon the precise cellular environment.
摘要：
β-catenin在慢性HBV感染的转基因小鼠模型中调节细胞培养物中的HBV转录和体内病毒生物合成。因此,重要的是要了解哪些转录因子活性被β-catenin共激活以增强HBV的生物合成。β-连环蛋白表达在核受体介导的HBV转录的背景下的影响最初在人胚肾细胞系中进行评估，HEK293T.报告基因和病毒复制测定显示，β-连环蛋白可以通过一些共同激活HBV转录，最主要的肝受体同源物1（LRH1），但不是所有的核受体已知激活病毒的生物合成。同样，β-catenin激活的核受体介导的HBV转录和复制在人肝癌细胞系,Huh7，主要通过其对法尼醇X受体α（FXRα）的作用。这些数据表明，β-连环蛋白可以增强核受体介导的HBV生物合成，但是各种转录因子的相对重要性取决于精确的细胞环境。
