ArticlePloS one2017
Impact of the structural integrity of the three-way junction of adenovirus VAI RNA on PKR inhibition.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Cleavage region organizes the structural architecture of the SINE-derived B2 repressive ribozyme.Communications biology · 2026Article
- African swine fever virus L11L interferes with antiviral responses by targeting the IRF3 and PKR.Cellular and molecular life sciences : CMLS · 2025Article
- Sampling globally and locally correct RNA 3D structures using Ernwin, SPQR and experimental SAXS data.Nucleic acids research · 2024Article
- RNA recognition by PKR during DNA virus infection.Journal of medical virology · 2024Review
- RNA 3D structure modeling by fragment assembly with small-angle X-ray scattering restraints.Bioinformatics (Oxford, England) · 2023Article
- Inhibition of PKR by Viruses.Frontiers in microbiology · 2021Review
- Human DDX17 Unwinds Rift Valley Fever Virus Non-Coding RNAs.International journal of molecular sciences · 2020Article
- Analytical ultracentrifuge: an ideal tool for characterization of non-coding RNAs.European biophysics journal : EBJ · 2020Review
- Orchestrated efforts on host network hijacking: Processes governing virus replication.Virulence · 2020Review
- Review
- FARFAR2: Improved De Novo Rosetta Prediction of Complex Global RNA Folds.Structure (London, England : 1993) · 2020Article
- Nanoscale Structure Determination of Murray Valley Encephalitis and Powassan Virus Non-Coding RNAs.Viruses · 2020Article
- Zinc-finger protein CNBP alters the 3-D structure of lncRNA Braveheart in solution.Nature communications · 2020Article
- Crystal structure of an adenovirus virus-associated RNA.Nature communications · 2019Article
- The search for a PKR code-differential regulation of protein kinase R activity by diverse RNA and protein regulators.RNA (New York, N.Y.) · 2019Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Highly structured RNA derived from viral genomes is a key cellular indicator of viral infection. In response, cells produce the interferon inducible RNA-dependent protein kinase (PKR) that, when bound to viral dsRNA, phosphorylates eukaryotic initiation factor 2α and attenuates viral protein translation. Adenovirus can evade this line of defence through transcription of a non-coding RNA, VAI, an inhibitor of PKR. VAI consists of three base-paired regions that meet at a three-way junction; an apical stem responsible for the interaction with PKR, a central stem required for inhibition, and a terminal stem. Recent studies have highlighted the potential importance of the tertiary structure of the three-way junction to PKR inhibition by enabling interaction between regions of the central and terminal stems. To further investigate the role of the three-way junction, we characterized the binding affinity and inhibitory potential of central stem mutants designed to introduce subtle alterations. These results were then correlated with small-angle X-ray scattering solution studies and computational tertiary structural models. Our results demonstrate that while mutations to the central stem have no observable effect on binding affinity to PKR, mutations that appear to disrupt the structure of the three-way junction prevent inhibition of PKR. Therefore, we propose that instead of simply sequestering PKR, a specific structural conformation of the PKR-VAI complex may be required for inhibition.
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