ArticleNature biotechnology2025
Near-cognate tRNAs increase the efficiency and precision of pseudouridine-mediated readthrough of premature termination codons.
Article in Nature biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- The role of RNA modifications in cancer translational control.RNA biology · 2026Review
- RNAViruses · 2026Review
- Programmable RNA acetylation with CRISPR-Cas13.Nature chemical biology · 2026Article
- A Ψ-Ψ codon-anticodon pairing in nonsense suppression and translational recoding.Nature chemical biology · 2026Article
- Engineering a photoactivatable A-to-I RNA base editor for gene therapy in vivo.Nature biotechnology · 2026Article
- ENSURE: the encyclopedia of suppressor tRNA with an AI assistant.Nucleic acids research · 2026Article
- Single-strand deaminase-assisted editing for functional RNA manipulation.Nature biotechnology · 2026Article
- CRISPR-free RNA base editing mediated PTC-readthrough restores hearing in mice with Otof nonsense mutation.Nature communications · 2025Article
- mRNA-based immunotherapy platform targeting endometrial cancer.Journal of translational medicine · 2025Article
- Targeted RNA base editing for therapeutic: mechanisms and advances.Pharmaceutical science advances · 2025Review
- Functions and therapeutic applications of pseudouridylation.Nature reviews. Molecular cell biology · 2025Review
- Optimization of ACE-tRNAs function in translation for suppression of nonsense mutations.Nucleic acids research · 2024Article
- Therapeutic Nonsense Suppression Modalities: From Small Molecules to Nucleic Acid-Based Approaches.Biomedicines · 2024Review
Corrections and comments
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9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Programmable RNA pseudouridylation has emerged as a new type of RNA base editor to suppress premature termination codons (PTCs) that can lead to truncated and nonfunctional proteins. However, current methods to correct disease-associated PTCs suffer from low efficiency and limited precision. Here we develop RESTART v3, which uses near-cognate tRNAs to improve the readthrough efficiency of pseudouridine-modified PTCs. We show an average of ~5-fold (range: 2.1- to 9.5-fold) higher editing efficiency than RESTART v2 in cultured cells and achieve functional PTC readthrough in disease cell models of cystic fibrosis and Hurler syndrome. Furthermore, RESTART v3 enables accurate incorporation of the original amino acid for nearly half of the PTC sites, considering the naturally occurring frequencies of sense-to-nonsense codons, without affecting normal termination codons. Although off-target sites were detected, we did not observe changes to the coding information or the expression level of transcripts, and the overall natural tRNA abundance remained constant.
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