ArticleNucleic acids research2014
The P body protein LSm1 contributes to stimulation of hepatitis C virus translation, but not replication, by microRNA-122.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Review
- 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
- miR-122 and Ago interactions with the HCV genome alter the structure of the viral 5' terminus.Nucleic acids research · 2019Article
- Rotavirus Induces Formation of Remodeled Stress Granules and P Bodies and Their Sequestration in Viroplasms To Promote Progeny Virus Production.Journal of virology · 2018Article
- Eukaryotic translation initiation factor 4AII contributes to microRNA-122 regulation of hepatitis C virus replication.Nucleic acids research · 2018Article
- Roles of the 5' Untranslated Region of Nonprimate Hepacivirus in Translation Initiation and Viral Replication.Journal of virology · 2018Article
- MicroRNA 130a Regulates both Hepatitis C Virus and Hepatitis B Virus Replication through a Central Metabolic Pathway.Journal of virology · 2018Article
- Signals Involved in Regulation of Hepatitis C Virus RNA Genome Translation and Replication.Frontiers in microbiology · 2018Review
- Differential hepatitis C virus RNA target site selection and host factor activities of naturally occurring miR-122 3΄ variants.Nucleic acids research · 2017Article
- Characterization of miR-122-independent propagation of HCV.PLoS pathogens · 2017Article
- Hepatitis C Virus Exploitation of Processing Bodies.Journal of virology · 2016Review
- 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
- Monitoring the spatiotemporal activities of miRNAs in small animal models using molecular imaging modalities.International journal of molecular sciences · 2015Review
- Novel viral translation strategies.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The P body protein LSm1 stimulates translation and replication of hepatitis C virus (HCV). As the liver-specific microRNA-122 (miR-122) is required for HCV replication and is associated with P bodies, we investigated whether regulation of HCV by LSm1 involves miR-122. Here, we demonstrate that LSm1 contributes to activation of HCV internal ribosome entry site (IRES)-driven translation by miR-122. This role for LSm1 is specialized for miR-122 translation activation, as LSm1 depletion does not affect the repressive function of miR-122 at 3' untranslated region (UTR) sites, or miR-122-mediated cleavage at a perfectly complementary site. We find that LSm1 does not influence recruitment of the microRNA (miRNA)-induced silencing complex to the HCV 5'UTR, implying that it regulates miR-122 function subsequent to target binding. In contrast to the interplay between miR-122 and LSm1 in translation, we find that LSm1 is not required for miR-122 to stimulate HCV replication, suggesting that miR-122 regulation of HCV translation and replication have different requirements. For the first time, we have identified a protein factor that specifically contributes to activation of HCV IRES-driven translation by miR-122, but not to other activities of the miRNA. Our results enhance understanding of the mechanisms by which miR-122 and LSm1 regulate HCV.
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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.