ArticleInternational journal of molecular sciences2023
Investigating the Inhibition of FTSJ1, a Tryptophan tRNA-Specific 2'-O-Methyltransferase by NV TRIDs, as a Mechanism of Readthrough in Nonsense Mutated CFTR.
Article in International journal of molecular sciences, 2023. 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, 12 citations in OpenAlex.
- Comparative evaluation of TRIDs : a strategy to improve treatments.Journal of translational medicine · 2026Article
- Beyond the stop: Oxadiazole TRIDs restore LRBA protein expression in nonsense-driven primary immunodeficiency.Molecular therapy. Nucleic acids · 2026Article
- QSAR-Guided Design of Serotonin Transporter Inhibitors Supported by Molecular Docking and Biased Molecular Dynamics.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Repurposing of lansoprazole and nitazoxanide as NR2F2 inhibitors in the gastric cancer cell line GCIY: computational insights and siRNA-mediatedFrontiers in chemistry · 2026Article
- Docking in the Dark: Insights into Protein-Protein and Protein-Ligand Blind Docking.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Review
- Advancing Therapeutic Strategies for Nonsense-Related Diseases: From Small Molecules to Nucleic Acid-Based Innovations.IUBMB life · 2025Review
- DNMT1 prolonged absence is a tunable cellular stress that triggers cell proliferation arrest to protect from major DNA methylation loss.Cellular and molecular life sciences : CMLS · 2024Article
- Promoting readthrough of nonsense mutations in CF mouse model: Biodistribution and efficacy of NV848 in rescuing CFTR protein expression.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Systematic deletion of symmetricalNAR molecular medicine · 2024Article
- tRNA modifications and tRNA-derived small RNAs: new insights of tRNA in human disease.Cell biology and toxicology · 2024Review
- Readthrough Activators and Nonsense-Mediated mRNA Decay Inhibitor Molecules: Real Potential in Many Genetic Diseases Harboring Premature Termination Codons.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Readthrough Approach Using NV Translational Readthrough-Inducing Drugs (TRIDs): A Study of the Possible Off-Target Effects on Natural Termination Codons (NTCs) on TP53 and Housekeeping Gene Expression.International journal of molecular sciences · 2023Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Cystic Fibrosis (CF) is an autosomal recessive genetic disease caused by mutations in the CFTR gene, coding for the CFTR chloride channel. About 10% of the CFTR gene mutations are "stop" mutations that generate a premature termination codon (PTC), thus synthesizing a truncated CFTR protein. A way to bypass PTC relies on ribosome readthrough, which is the ribosome's capacity to skip a PTC, thus generating a full-length protein. "TRIDs" are molecules exerting ribosome readthrough; for some, the mechanism of action is still under debate. We investigate a possible mechanism of action (MOA) by which our recently synthesized TRIDs, namely NV848, NV914, and NV930, could exert their readthrough activity by in silico analysis and in vitro studies. Our results suggest a likely inhibition of FTSJ1, a tryptophan tRNA-specific 2'-O-methyltransferase.
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Registered trials
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