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损伤特异性DNA结合蛋白1(DDB1)的敲低增强了HBx-siRNA介导的对乙肝病毒复制的抑制作用。

Knockdown of damage-specific DNA binding protein 1 (DDB1) enhances the HBx-siRNA-mediated inhibition of HBV replication.

作者信息

Tang Kai-Fu, Xie Jing, Chen Min, Liu Qi, Zhou Xi-Yuan, Zeng Weiqun, Huang Ai-Long, Zuo Guo-qing, Wang Yan, Xiang Rong, Ren Hong

机构信息

Key Laboratory of Molecular Biology for Infectious Diseases, Ministry of Education, Institute for Viral Hepatitis, The Second Affiliated Hospital, Chongqing University of Medical Sciences, Chongqing 400010, PR China.

出版信息

Biologicals. 2008 May;36(3):177-83. doi: 10.1016/j.biologicals.2007.11.002. Epub 2008 Mar 4.

Abstract

Recent studies have demonstrated that the effect of inhibition of HBV replication can be achieved by RNA interference (RNAi) at both the cellular and organismal levels. However, HBV replication cannot be completely inhibited by this method. To completely inhibit HBV replication, new strategies for improving the inhibition efficacy of HBV-specific siRNAs are needed. In this study, we demonstrated that knockdown of damage-specific DNA binding protein 1(DDB1), a protein involved in nucleotide-excision repair and HBV replication, significantly enhanced the HBx-siRNA-mediated inhibition of HBV replication. Although knockdown of DDB1 may be toxic to normal liver cells, our results indeed suggest a new direction to enhance the efficacy of HBV-siRNA-mediated inhibition of HBV replication.

摘要

最近的研究表明,通过RNA干扰(RNAi)在细胞和机体水平上均可实现抑制乙肝病毒(HBV)复制的效果。然而,该方法无法完全抑制HBV复制。为了完全抑制HBV复制,需要新的策略来提高HBV特异性小干扰RNA(siRNA)的抑制效果。在本研究中,我们证明了损伤特异性DNA结合蛋白1(DDB1)(一种参与核苷酸切除修复和HBV复制的蛋白质)的敲低显著增强了HBx-siRNA介导的HBV复制抑制作用。尽管敲低DDB1可能对正常肝细胞有毒性,但我们的结果确实为提高HBV-siRNA介导的HBV复制抑制效果指明了一个新方向。

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