期刊
JOURNAL OF VIROLOGY
卷 86, 期 18, 页码 10221-10225出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00882-12
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资金
- Midwest Regional Center of Excellence for Biodefense and Emerging Infectious Diseases Research [5U54AI057160]
- National Institutes of Health [DK081817, AI065535]
We have examined the underlying mechanism of hepatitis C virus (HCV)-mediated IFITM1 regulation. IFITM1 is a potential target of miR-130a. Our results demonstrated that miR-130a expression was significantly higher in HCV-infected hepatocytes and liver biopsy specimens than in controls. Introduction of anti-miR-130a in hepatocytes increased IFITM1 expression. Hepatocytes stably expressing IFITM1 reduced HCV replication. Together, these results suggested that HCV infection of hepatocytes upregulates miR-130a and that use of anti-miR-130a may have potential for restriction of HCV replication.
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