ArticleThe Journal of general virology2015
Translational readthrough-promoting drugs enhance pseudoknot-mediated suppression of the stop codon at the Moloney murine leukemia virus gag–pol junction.
Article in The Journal of general virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Mechanism of read-through enhancement by aminoglycosides and mefloquine.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genome-scale quantification and prediction of pathogenic stop codon readthrough by small molecules.Nature genetics · 2024Article
- Retroviral RNA Processing.Viruses · 2022Review
- Cellular senescence limits translational readthrough.Biology open · 2021Article
- RNA-based therapies in animal models of Leber congenital amaurosis causing blindness.Precision clinical medicine · 2020Article
- How to get away with nonsense: Mechanisms and consequences of escape from nonsense-mediated RNA decay.Wiley interdisciplinary reviews. RNA · 2020Review
- Interrogation of Eukaryotic Stop Codon Readthrough Signals by in Vitro RNA Selection.Biochemistry · 2019Article
- Functional and structural characterization of the chikungunya virus translational recoding signals.The Journal of biological chemistry · 2018Article
- Ataluren stimulates ribosomal selection of near-cognate tRNAs to promote nonsense suppression.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Translational readthrough-promoting drugs enhance the incorporation of amino acids at stop codons and can thus bypass premature termination during protein synthesis. The polymerase (Pol) proteins of Moloney murine leukemia virus (MoMLV) are synthesized as a large Gag–Pol fusion protein, formed by the readthrough of a stop codon at the end of the gag ORF. The downstream pol ORF lacks its own start codon, and Pol protein synthesis is wholly dependent on translation of the upstream gag gene and the readthrough event for expression. Here, we explored the effects of readthrough-promoting drugs – aminoglycoside antibiotics and the small molecule ataluren – on the efficiency of readthrough of the stop codon in the context of the MoMLV genome. We showed that these compounds increased readthrough of the stop codon at the MoMLV gag–pol junction in vivo above the already high basal level and that the resulting elevated gag–pol readthrough had deleterious effects on virus replication. We also showed that readthrough efficiency could be driven to even higher levels in vitro, and that the combination of the small molecules and the RNA structure at the MoMLV stop codon could achieve extremely high readthrough efficiencies.
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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.