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IR@PKUHSC  > 北京大学第二临床医学院  > 北京大学肝病研究所  > 期刊论文
学科主题: 临床医学
题名:
Role of ISGF3 in modulating the anti-hepatitis B virus activity of interferon-alpha in vitro
作者: Zhang, Quan; Wang, Yan; Wei, Lai; Jiang, Dong; Wang, Jiang Hua; Rao, Hui Ying; Zhu, Ling; Chen, Hongsong; Fei, Ran; Cong, Xu
关键词: gene chip ; hepatitis B virus ; interferon-alpha ; signal transducers and activators of transcription proteins ; signal transduction
刊名: JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
发表日期: 2008-11-01
DOI: 10.1111/j.1440-1746.2007.04985.x
卷: 23, 期:11, 页:1747-1761
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Gastroenterology & Hepatology
研究领域[WOS]: Gastroenterology & Hepatology
关键词[WOS]: TYROSINE-PHOSPHORYLATED STAT1 ; GENE-EXPRESSION ; SIGNAL-TRANSDUCTION ; ANTIVIRAL TREATMENT ; PROTEIN ; ACTIVATION ; INFECTION ; PATHWAYS ; DNA ; TRANSCRIPTION
英文摘要:

Although interferon-alpha (IFN-alpha) is an effective treatment for hepatitis B virus (HBV) infection, its precise mechanism of action has not been identified. In this study, we investigated the role of signal transduction pathways in the activation of anti-HBV responses mediated by IFN-alpha.

Using an oligo microarray, we found that four genes in the IFN-alpha signal pathway were markedly upregulated by IFN-alpha in human hepatoma cells regardless of whether they had been transfected with a plasmid containing the HBV genome: signal transducers and activators of transcription 1 (STAT1), interferon regulatory factor-9 (IRF-9, also called ISGF3 gamma or P48), IFN-alpha-inducible protein 15 (IFI-15) and IFN-alpha-inducible protein 6-16 (IFI-6-16). We also investigated the role of IFN-stimulated gene factor3 (ISGF3) complex in IFN-alpha-mediated anti-HBV responses in human hepatoma cells by measuring the mRNA of the three genes within ISGF3 (STAT1, STAT2 and IRF-9) using semiquantitative reverse-transcription PCR (RT-PCR), and expression of the three proteins by western blot, and the mRNA and protein of dsRNA-dependent protein kinase (PKR).

STAT1, STAT2, IRF-9 and PKR mRNA as well as protein levels were upregulated by IFN-alpha treatment. When cells were pretreated with genistein, STAT1, STAT2 and IRF-9 mRNA levels remained unchanged after IFN-alpha stimulation, but PKR mRNA levels decreased, and the expression of the STAT1, P-STAT2, IRF-9 and PKR proteins decreased. Levels of HBV DNA decreased in the supernatants of cells treated with IFN-alpha, while ISGF3 levels increased. The quantity of HBV DNA remained unchanged by pretreating with genistein.

These observations suggested that the Janus tyrosine kinase-STAT (JAK-STAT) pathway may play a major role in mediating the effects of IFN-alpha against HBV, and that ISGF3 might be a key factor.

语种: 英语
所属项目编号: 2005BC522902 ; H030230280410 ; 30571693
项目资助者: Major State Basic Research Development Program of China ; Beijing Municipal Science and Technology Commission ; National Natural Science Foundation of China
WOS记录号: WOS:000261115000024
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/51611
Appears in Collections:北京大学第二临床医学院_北京大学肝病研究所_期刊论文

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作者单位: Peking Univ, Inst Hepatol, Peoples Hosp, Beijing 100044, Peoples R China

Recommended Citation:
Zhang, Quan,Wang, Yan,Wei, Lai,et al. Role of ISGF3 in modulating the anti-hepatitis B virus activity of interferon-alpha in vitro[J]. JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY,2008,23(11):1747-1761.
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