miR-125b inhibits hepatitis B virus expression in vitro through targeting of the SCNN1A gene
Archives of Virology, ISSN: 1432-8798, Vol: 159, Issue: 12, Page: 3335-3343
2014
- 38Citations
- 21Captures
- 1Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations38
- Citation Indexes38
- 38
- CrossRef17
- Captures21
- Readers21
- 21
- Mentions1
- News Mentions1
- 1
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Article Description
microRNAs (miRNAs) are small noncoding RNAs that modulate gene expression at the posttranscriptional level, playing an important role in many diseases. However, reports concerning the role of miRNA in hepatitis B virus (HBV) infection are limited. miRNA chips were used to investigate miRNA changes during HBV infection in vitro. Bioinformatics analysis was used to explore possible miRNA and target genes during HBV infection. The expression of miR-125b and its potential target gene, sodium channel, non-voltage-gated 1 alpha (SCNN1A), was further analyzed. A total of 136 miRNAs were analyzed in an HBV transient transfection model (HepG2-HBV1.3), and 78 miRNAs were differentially expressed in HepG2.2.15 cells compared with HepG2 cells. miR-125b expression was decreased in both HepG2-HBV1.3 and HepG2.2.15 cells, and ectopic expression of miR-125b inhibited HBV DNA intermediates and secretion of HBsAg and HBeAg. miR-125b also inhibited the mRNA and protein levels of SCNN1A. Using a dual luciferase reporter system, we found that SCNN1A was one of the targets of miR-125b. In this study, we found that miR-125b inhibits HBV expression in vitro by regulating SCNN1A expression.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84919921757&origin=inward; http://dx.doi.org/10.1007/s00705-014-2208-y; http://www.ncbi.nlm.nih.gov/pubmed/25173609; http://link.springer.com/10.1007/s00705-014-2208-y; https://dx.doi.org/10.1007/s00705-014-2208-y; https://link.springer.com/article/10.1007/s00705-014-2208-y
Springer Science and Business Media LLC
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