ArticleNature medicine1996
Aminoglycoside antibiotics restore CFTR function by overcoming premature stop mutations.
Article in Nature medicine, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 3 of them syntheses that pooled it.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
175 citing papers in PubMed, 3 syntheses or guidelines pooled it, 493 citations in OpenAlex.
- Ataluren and similar compounds (specific therapies for premature termination codon class I mutations) for cystic fibrosis.The Cochrane database of systematic reviews · 2023Pooled it
- A Systematic Review of the Clinical Efficacy and Safety of CFTR Modulators in Cystic Fibrosis.Scientific reports · 2019Pooled it
- Ataluren and similar compounds (specific therapies for premature termination codon class I mutations) for cystic fibrosis.The Cochrane database of systematic reviews · 2017Pooled it
- No detectable improvements in cystic fibrosis transmembrane conductance regulator by nasal aminoglycosides in patients with cystic fibrosis with stop mutations.American journal of respiratory cell and molecular biology · 2007Trial
- In vitro prediction of stop-codon suppression by intravenous gentamicin in patients with cystic fibrosis: a pilot study.BMC medicine · 2007Trial
- Translating biosynthetic gene cluster architecture into biosensor design for microbial natural product discovery.Essays in biochemistry · 2026Review
- Functional Characterization of a Novel Intronic Complement Factor I Variant in Factor I Deficiency and Atypical Hemolytic Uremic Syndrome.Kidney international reports · 2026Article
- Identification of small molecules that enhance aminoglycoside-mediated suppression ofMolecular therapy. Oncology · 2026Article
- Enhancing RNA base editing on mammalian transcripts with small nuclear RNAs.Nature chemical biology · 2026Article
- RFFL-mediated protein quality control limits functional rescue of TRID-CFTR modulator combination therapy for cystic fibrosis nonsense mutations.Cellular and molecular life sciences : CMLS · 2026Article
- Identity, functional consequences, and context effects of amino acids inserted during suppression of CFTR nonsense mutations.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2026Article
- Review
- Defining the high-translational readthrough stop codon context.PLoS genetics · 2025Article
- Advancing Therapeutic Strategies for Nonsense-Related Diseases: From Small Molecules to Nucleic Acid-Based Innovations.IUBMB life · 2025Review
- Exploring the therapeutic potential of modulating nonsense-mediated mRNA decay.RNA (New York, N.Y.) · 2025Review
- Combinatorial biosynthesis of novel gentamicin derivatives with nonsense mutation readthrough activity and low cytotoxicity.Frontiers in pharmacology · 2025Article
- Near-cognate tRNAs increase the efficiency and precision of pseudouridine-mediated readthrough of premature termination codons.Nature biotechnology · 2025Article
- Optimization of ACE-tRNAs function in translation for suppression of nonsense mutations.Nucleic acids research · 2024Article
- Cystic Fibrosis: A Journey through Time and Hope.International journal of molecular sciences · 2024Review
- Genome-scale quantification and prediction of pathogenic stop codon readthrough by small molecules.Nature genetics · 2024Article
115 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystic fibrosis (CF) is caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR). A single recessive mutation, the deletion of phenylalanine 508 (deltaF508), causes severe CF and resides on 70% of mutant chromosomes. Severe CF is also caused by premature stop mutations, which are found on 5% of CF chromosomes. Here we report that two common, disease-associated stop mutations can be suppressed by treating cells with low doses of the aminoglycoside antibiotic G-418. Aminoglycoside treatment resulted in the expression of full-length CFTR and restored its cyclic AMP-activated chloride channel activity. Another aminoglycoside, gentamicin, also promoted the expression of full-length CFTR. These results suggest that treatment with aminoglycosides may provide a means of restoring CFTR function in patients with this class of mutation.
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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.