ArticleNature communications2025
AAV-delivered engineered suppressor tRNA rescues visual function in mice with an inherited retinal disease.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed.
- Programmed repair of disease-causing UGA premature termination codons in mammalian brain.Nucleic acids research · 2026Article
- Engineered tRNA reduces vision loss in a mouse model of Leber congenital amaurosis.Signal transduction and targeted therapy · 2026Article
- Tetrahedral DNA nanostructure-delivered suppressor tRNA ameliorates nephropathy inNAR molecular medicine · 2026Article
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
Nonsense mutations change a sense codon into a premature termination codon (PTC) in mRNA and account for approximately 18.5% of human inherited retinal diseases (IRDs)-related mutation. Nonsense suppression therapies by small molecular drugs or suppressor tRNAs (sup-tRNAs) can introduce an amino acid at PTC, thereby promoting the production of full-length proteins. While sup-tRNA-based therapies have shown promising results in cell culture models, challenges remain for in vivo delivery, particularly regarding efficacy, stability, and safety. In this study, we engineer the body sequence of sup-tRNA
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