ArticleMolecular therapy. Nucleic acids2023
Transfer RNA-mediated restoration of potassium current and electrical correction in premature termination long-QT syndrome hERG mutants.
Article in Molecular therapy. Nucleic acids, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- 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
- The regulation, function and disease relevance of cytoplasmic tRNAs.Nature reviews. Molecular cell biology · 2026Review
- Anticodon-edited transfer RNAs (ACE-tRNAs) encoded as therapeutic nonviral minimal DNA vectors.Nucleic acids research · 2026Article
- Precision therapeutic tRNA rescue of nonsense mutation R166X inJournal of precision medicine (Amsterdam, Netherlands) · 2025Article
- Anticodon Edited Transfer RNAs (ACE-tRNAs) Encoded as Therapeutic Nonviral Minimal DNA Vectors.bioRxiv : the preprint server for biology · 2025Article
- ACE-tRNAs are a platform technology for suppressing nonsense mutations that cause cystic fibrosis.Nucleic acids research · 2025Article
- Mechanism-based approach in designing patient-specific combination therapies for nonsense mutation diseases.Nucleic acids research · 2025Article
- Anticodon-edited tRNA enables translational readthrough of COL4A5 premature termination codons.PloS one · 2025Article
- Optimization of ACE-tRNAs function in translation for suppression of nonsense mutations.Nucleic acids research · 2024Article
- Mechanism-based approach in designing patient-specific combination therapies for nonsense mutation diseases.bioRxiv : the preprint server for biology · 2024Article
- Suppressor tRNAs at the interface of genetic code expansion and medicine.Frontiers in genetics · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Disease-causing premature termination codons (PTCs) individually disrupt the functional expression of hundreds of genes and represent a pernicious clinical challenge. In the heart, loss-of-function mutations in the hERG potassium channel account for approximately 30% of long-QT syndrome arrhythmia, a lethal cardiac disorder with limited treatment options. Premature termination of ribosomal translation produces a truncated and, for potassium channels, a potentially dominant-negative protein that impairs the functional assembly of the wild-type homotetrameric hERG channel complex. We used high-throughput flow cytometry and patch-clamp electrophysiology to assess the trafficking and voltage-dependent activity of hERG channels carrying patient PTC variants that have been corrected by anticodon engineered tRNA. Adenoviral-mediated expression of mutant hERG channels in cultured adult guinea pig cardiomyocytes prolonged action potential durations, and this deleterious effect was corrected upon adenoviral delivery of a human Arg
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