ArticlePloS one2013
Modulation of hepatitis C virus RNA accumulation and translation by DDX6 and miR-122 are mediated by separate mechanisms.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Review
- Cellular factors involved in the hepatitis C virus life cycle.World journal of gastroenterology · 2021Review
- The Role of the Liver-Specific microRNA, miRNA-122 in the HCV Replication Cycle.International journal of molecular sciences · 2020Review
- Effect of P-body component Mov10 on HCV virus production and infectivity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Hepatitis C Virus Translation Regulation.International journal of molecular sciences · 2020Review
- Review
- Impact of a patient-derived hepatitis C viral RNA genome with a mutated microRNA binding site.PLoS pathogens · 2019Article
- Eukaryotic translation initiation factor 4AII contributes to microRNA-122 regulation of hepatitis C virus replication.Nucleic acids research · 2018Article
- Signals Involved in Regulation of Hepatitis C Virus RNA Genome Translation and Replication.Frontiers in microbiology · 2018Review
- DDX6 Represses Aberrant Activation of Interferon-Stimulated Genes.Cell reports · 2017Article
- Translation control: Learning from viruses, again.RNA biology · 2017Article
- Cellular DEAD-box RNA helicase DDX6 modulates interaction of miR-122 with the 5' untranslated region of hepatitis C virus RNA.Virology · 2017Article
- Zika virus disrupts molecular fingerprinting of human neurospheres.Scientific reports · 2017Article
- A novel translational control mechanism involving RNA structures within coding sequences.Genome research · 2017Article
- Review
- Regulation of Hepatitis C Virus Genome Replication by Xrn1 and MicroRNA-122 Binding to Individual Sites in the 5' Untranslated Region.Journal of virology · 2015Article
- Cytoplasmic RNA Granules and Viral Infection.Annual review of virology · 2014Article
- Epigenetic mechanisms underlying the link between non-alcoholic fatty liver diseases and nutrition.Nutrients · 2014Review
- Understanding the interaction of hepatitis C virus with host DEAD-box RNA helicases.World journal of gastroenterology · 2014Review
- DDX6 localizes to nuage structures and the annulus of mammalian spermatogenic cells.Histochemistry and cell biology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
DDX6 and other P-body proteins are required for efficient replication of Hepatitis C Virus (HCV) by unknown mechanisms. DDX6 has been implicated in miRNA induced gene silencing, and since efficient HCV replication and translation relies on the cellular microRNA, miR-122, we hypothesized that DDX6 had a role in the mechanism of action of miR-122. However, by using multiple HCV translation and replication assays we have found this is not the case. DDX6 silencing decreased HCV replication and translation, but did not affect the ability of miR-122 to stimulate HCV translation or promote HCV RNA accumulation. In addition, the negative effect of DDX6 silencing on HCV replication and translation was not dependent on miR-122 association with the HCV genome. Thus, DDX6 does not have a role in the activity of miR-122, and it appears that DDX6 and miR-122 modulate HCV through distinct pathways. This effect was seen in both Huh7.5 cells and in Hep3B cells, indicating that the effects are not cell type specific. Since infections by other viruses in the Flaviviridae family, including Dengue and West Nile Virus, also disrupt P-bodies and are regulated by DDX6, we speculate that DDX6 may have a common function that support the replication of several Flaviviruses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.