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您的检索式：作者名="Zhikui Cheng"
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| 1 | Inhibition of hepatitis B virus replication by quercetin in human hepatoma cell lines显示文摘Hepatitis B virus(HBV) infection is one of the most serious and prevalent viral diseases in the world. Although several anti-HBV drugs have been used clinically, their side and adverse effects limit treatment efficacy. Therefore, it is necessary to identify novel potential anti-HBV agents. The flavonol quercetin has shown activity against some retroviruses, but its effect on HBV remains unclear. In the present study, quercetin was incubated with Hep G2.2.15 cells, as well as Hu H-7 cells transfected with an HBV plasmid. Quercetin was shown to significantly reduce Hepatitis B surface antigen(HBs Ag) and Hepatitis B e antigen(HBe Ag), secretion and HBV genomic DNA levels in both cell lines. In addition, co-incubation with lamivudine(3TC), entecavir(ETV), or adefovir(Ade) further enhanced the quercetin-induced inhibition of HBV replication. This inhibition was partially associated with decreased heat shock proteins and HBV transcription levels. The results indicate that quercetin inhibited HBV antigen secretion and genome replication in human hepatoma cell lines, which suggests that quercetin may be a potentially effective anti-HBV agent. | Zhikui Cheng Ge Sun Wei Guo Yayun Huang Weihua Sun Fei Zhao Kanghong Hu | 2015 | Virologica Sinica2015，30，4： | 20 |
| 2 | GCN5 Acetyltransferase Inhibits PGC1α-induced Hepatitis B Virus Biosynthesis显示文摘Hepatitis B virus (HBV) biosynthesis is primarily restricted to hepatocytes due to the governing of liver-enriched nuclear receptors (NRs) on viral RNA synthesis. The liver-enriched NR hepatocyte nuclear factor 4α (HNF4α), the key regulator of genes implicated in hepatic glucose metabolism, is also a primary determinant of HBV pregenomic RNA synthesis and HBV replication. Peroxisome proliferator-activated receptor-γ coactivator 1α (PGC1α) coactivates and further enhances the effect of HNF4α on HBV biosynthesis. Here, we showed that the acetyltransferase General Control Non-repressed Protein 5 (GCN5) acetylated PGC1α, leading to alteration of PGC1α from a transcriptionally active state into an inactive state. As a result, the coactivation activity of PGC1α on HBV transcription and replication was suppressed. Apparently, an acetylation site mutant of PGC1α (PGC1αR13) still had coactivation activity as GCN5 could not suppress the coactivation activity of the mutant. Moreover, a catalytically inactive acetyltransferase mutant GCN5m, due to the loss of acetylation activity, failed to inhibit the coactivation function of PGC1α in HBV biosynthesis. Our results demonstrate that GCN5, through its acetyltransferase activity, inhibits PGC1α-induced enhancement of HBV transcription and replication both in vitro and in vivo. | Xiaohui Tian Fei Zhao Zhikui Cheng Ming Zhou Xiaoguang Zhi Jiafu Li Kanghong Hu | 2013 | Virologica Sinica2013，28，4： | 2 |
| 3 | Virus-inducible IGFALS facilitates innate immune responses by mediating IRAK1 and TRAF6 activation显示文摘Activation of TLR signaling is a first line of the host defense system in the elimination of invading pathogens.1 Insulin-like growth factor binding protein, acid-labile subunit (IGFALS) is a leucine-rich glycoprotein. By prolonging the half-life of IGF-I in the vascular system,2 IGFALS regulates the bioavailability of IGF, which is crucial for normal growth and development and metabolic regulation.3,4 However, the role of IGFALS in antiviral innate immune responses has not been established. In this study, we found that IGFALS is virus inducible, while it in turn inhibits viral replication. Mechanistically, IGFALS directly associates with IRAK1 and TRAF6, facilitating IRAK1/TRAF6 complex formation and enhancing K63-linked polyubiquitination of both proteins for full activation, thereby facilitating antiviral signaling. | Gang Xu Feiyan Deng Qi Zuo Lin Liu Kaiwen Dou Zhikui Cheng Wei Cao Chuanjin Luo Chen Yu Shi Liu Ying Zhu | 2021 | Cellular & Molecular Immunology2021，18，6： | 0 |
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