ArticleJournal of cell science2017
Premature termination codon readthrough in human cells occurs in novel cytoplasmic foci and requires UPF proteins.
Article in Journal of cell science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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Who cites it
12 citing papers in PubMed.
- Comparative evaluation of TRIDs : a strategy to improve treatments.Journal of translational medicine · 2026Article
- Developing AAV-delivered nonsense suppressor tRNAs for neurological disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- Readthrough Activators and Nonsense-Mediated mRNA Decay Inhibitor Molecules: Real Potential in Many Genetic Diseases Harboring Premature Termination Codons.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Identifying Potent Nonsense-Mediated mRNA Decay Inhibitors with a Novel Screening System.Biomedicines · 2023Article
- Recoding of Nonsense Mutation as a Pharmacological Strategy.Biomedicines · 2023Review
- Diverse Roles of the Exon Junction Complex Factors in the Cell Cycle, Cancer, and Neurodevelopmental Disorders-Potential for Therapeutic Targeting.International journal of molecular sciences · 2022Review
- Comprehensive Analysis of Combinatorial Pharmacological Treatments to Correct Nonsense Mutations in the CFTR Gene.International journal of molecular sciences · 2021Article
- Nonsense-mediated RNA decay and its bipolar function in cancer.Molecular cancer · 2021Review
- How to get away with nonsense: Mechanisms and consequences of escape from nonsense-mediated RNA decay.Wiley interdisciplinary reviews. RNA · 2020Review
- Translation Termination and Ribosome Recycling in Eukaryotes.Cold Spring Harbor perspectives in biology · 2018Review
- Review
- Optimized approach for the identification of highly efficient correctors of nonsense mutations in human diseases.PloS one · 2017Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Nonsense-mutation-containing messenger ribonucleoprotein particles (mRNPs) transit through cytoplasmic foci called P-bodies before undergoing nonsense-mediated mRNA decay (NMD), a cytoplasmic mRNA surveillance mechanism. This study shows that the cytoskeleton modulates transport of nonsense-mutation-containing mRNPs to and from P-bodies. Impairing the integrity of cytoskeleton causes inhibition of NMD. The cytoskeleton thus plays a crucial role in NMD. Interestingly, disruption of actin filaments results in both inhibition of NMD and activation of premature termination codon (PTC) readthrough, while disruption of microtubules causes only NMD inhibition. Activation of PTC readthrough occurs concomitantly with the appearance of cytoplasmic foci containing UPF proteins and mRNAs with nonsense mutations but lacking the P-body marker DCP1a. These findings demonstrate that in human cells, PTC readthrough occurs in novel 'readthrough bodies' and requires the presence of UPF proteins.
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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.