ArticleJournal of virology2008
Mutation of mapped TIA-1/TIAR binding sites in the 3' terminal stem-loop of West Nile virus minus-strand RNA in an infectious clone negatively affects genomic RNA amplification.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 58 citations in OpenAlex.
- Cellular Biology: Virus-Host Interactions and RNA Structure and Function.Current topics in microbiology and immunology · 2026Review
- Sensing nucleotide composition in virus RNA.Bioscience reports · 2023Review
- RNA binding protein TIAR modulates HBV replication by tipping the balance of pgRNA translation.Signal transduction and targeted therapy · 2023Article
- Mutagenesis and structural studies reveal the basis for the specific binding of SARS-CoV-2 SL3 RNA element with human TIA1 protein.Nature communications · 2023Article
- Positive strand RNA viruses differ in the constraints they place on the folding of their negative strand.RNA (New York, N.Y.) · 2022Article
- T-Cell Intracellular Antigen 1-Like Protein in Physiology and Pathology.International journal of molecular sciences · 2022Review
- The Multifunctional Faces of T-Cell Intracellular Antigen 1 in Health and Disease.International journal of molecular sciences · 2022Review
- Two Interferon-Stimulated Response Elements Cooperatively Regulate Interferon-Stimulated Gene Expression in West Nile Virus-Infected IFNARJournal of virology · 2021Article
- The Nuclear Pore Complex Is a Key Target of Viral Proteases to Promote Viral Replication.Viruses · 2021Review
- Universal RNAFrontiers in microbiology · 2020Review
- Structures and Functions of the 3' Untranslated Regions of Positive-Sense Single-Stranded RNA Viruses Infecting Humans and Animals.Frontiers in cellular and infection microbiology · 2020Review
- Zika Virus Subverts Stress Granules To Promote and Restrict Viral Gene Expression.Journal of virology · 2019Article
- Stress Granules and Processing Bodies in Translational Control.Cold Spring Harbor perspectives in biology · 2019Review
- Inhibition of Stress Granule Formation by Middle East Respiratory Syndrome Coronavirus 4a Accessory Protein Facilitates Viral Translation, Leading to Efficient Virus Replication.Journal of virology · 2018Article
- Biochemistry and Molecular Biology of Flaviviruses.Chemical reviews · 2018Review
- The Multiples Fates of the Flavivirus RNA Genome During Pathogenesis.Frontiers in genetics · 2018Review
- Review
- Spectral and Hydrodynamic Analysis of West Nile Virus RNA-Protein Interactions by Multiwavelength Sedimentation Velocity in the Analytical Ultracentrifuge.Analytical chemistry · 2017Article
- Zika virus produces noncoding RNAs using a multi-pseudoknot structure that confounds a cellular exonuclease.Science (New York, N.Y.) · 2016Article
- Structured RNAs that evade or confound exonucleases: function follows form.Current opinion in structural biology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Previous data showed that the cellular proteins TIA-1 and TIAR bound specifically to the West Nile virus 3' minus-strand stem-loop [WNV3'(-)SL] RNA (37) and colocalized with flavivirus replication complexes in WNV- and dengue virus-infected cells (21). In the present study, the sites on the WNV3'(-)SL RNA required for efficient in vitro T-cell intracellular antigen-related (TIAR) and T-cell intracellular antigen-1 (TIA-1) protein binding were mapped to short AU sequences (UAAUU) located in two internal loops of the WNV3'(-)SL RNA structure. Infectious clone RNAs with all or most of the binding site nucleotides in one of the 3' (-)SL loops deleted or substituted did not produce detectable virus after transfection or subsequent passage. With one exception, deletion/mutation of a single terminal nucleotide in one of the binding sequences had little effect on the efficiency of protein binding or virus production, but mutation of a nucleotide in the middle of a binding sequence reduced both the in vitro protein binding efficiency and virus production. Plaque size, intracellular genomic RNA levels, and virus production progressively decreased with decreasing in vitro TIAR/TIA-1 binding activity, but the translation efficiency of the various mutant RNAs was similar to that of the parental RNA. Several of the mutant RNAs that inefficiently interacted with TIAR/TIA-1 in vitro rapidly reverted in vivo, indicating that they could replicate at a low level and suggesting that an interaction between TIAR/TIA-1 and the viral 3'(-)SL RNA is not required for initial low-level symmetric RNA replication but instead facilitates the subsequent asymmetric amplification of genome RNA from the minus-strand template.
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Registered trials
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