ArticlePloS one2015
HuR and Ago2 Bind the Internal Ribosome Entry Site of Enterovirus 71 and Promote Virus Translation and Replication.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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
32 citing papers in PubMed, 41 citations in OpenAlex.
- Review
- RNP interfaces as regulatory "active sites": a repurposing strategy for small molecules targeting viral 5'-untranslated regions.Frontiers in molecular biosciences · 2026Article
- SFTSV NSs interacts with AGO2 to regulate the RNAi pathway for viral replication.Journal of virology · 2025Article
- m7G gene expression and disease risk model construction in patients with herpes zoster.Scientific reports · 2025Article
- Insight into the Life Cycle of Enterovirus-A71.Viruses · 2025Review
- Coxsackievirus B3-Induced mMicroorganisms · 2024Article
- Enterovirus evolution reveals the mechanism of an RNA-targeted antiviral and determinants of viral replication.Science advances · 2024Article
- CRISPR/Cas9-Mediated Knockout of theMicroorganisms · 2024Article
- Review
- Advances and Breakthroughs in IRES-Directed Translation and Replication of Picornaviruses.mBio · 2023Review
- Roles and mechanisms of exosomal microRNAs in viral infections.Archives of virology · 2023Review
- Identification of potential proteins translated from circular RNA splice variants.European journal of cell biology · 2023Article
- Article
- Review
- Host Restrictive Factors Are the Emerging Storm Troopers Against Enterovirus: A Mini-Review.Frontiers in immunology · 2022Review
- Heat Shock Protein A6, a Novel HSP70, Is Induced During Enterovirus A71 Infection to Facilitate Internal Ribosomal Entry Site-Mediated Translation.Frontiers in microbiology · 2021Article
- Functional analyses of mammalian virus 5'UTR-derived, small RNAs that regulate virus translation.Methods (San Diego, Calif.) · 2020Article
- Integrated approaches to reveal mechanisms by which RNA viruses reprogram the cellular environment.Methods (San Diego, Calif.) · 2020Review
- Editorial for "Methods to characterize virus small RNAs and RNA structures".Methods (San Diego, Calif.) · 2020Article
- IRES-targeting small molecule inhibits enterovirus 71 replication via allosteric stabilization of a ternary complex.Nature communications · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
EV71 (enterovirus 71) RNA contains an internal ribosomal entry site (IRES) that directs cap-independent initiation of translation. IRES-dependent translation requires the host's translation initiation factors and IRES-associated trans-acting factors (ITAFs). We reported recently that mRNA decay factor AUF1 is a negative-acting ITAF that binds IRES stem-loop II. We also reported that the small RNA-processing enzyme Dicer produces at least four small RNAs (vsRNAs) from the EV71 IRES. One of these, vsRNA1, derived from IRES stem-loop II, reduces IRES activity and virus replication. Since its mechanism of action is unknown, we hypothesized that it might control association of ITAFs with the IRES. Here, we identified the mRNA stability factor HuR and the RISC subunit Argonaute 2 (Ago2) as two ITAFs that bind stem-loop II. In contrast to AUF1, HuR and Ago2 promote EV71 IRES activity and virus replication. In vitro RNA-binding assays revealed that vsRNA1 can alter association of Ago2, HuR, and AUF1 with stem-loop II. This presents a possible mechanism by which vsRNA1 could control viral translation and replication.
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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.