ArticleScientific reports2017
mRNAs containing NMD-competent premature termination codons are stabilized and translated under UPF1 depletion.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
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- An alternative cytoplasmic SFPQ isoform with reduced phase separation potential is up-regulated in ALS.Science advances · 2025Article
- Variability in proliferative and migratory defects in Hirschsprung disease-associated RET pathogenic variants.American journal of human genetics · 2025Article
- The Suppression of Signal Transducer and Activator of Transcription-3 in A549 human Lung Carcinoma Cells Induced by Marine SpongeJournal of experimental pharmacology · 2025Article
- Variability in proliferative and migratory defects in Hirschsprung disease-associatedbioRxiv : the preprint server for biology · 2024Article
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- Nonsense-mediated mRNA decay uses complementary mechanisms to suppress mRNA and protein accumulation.Life science alliance · 2022Article
- Splicing modulators elicit global translational repression by condensate-prone proteins translated from introns.Cell chemical biology · 2022Article
- Nuclear SR-protein mediated mRNA quality control is continued in cytoplasmic nonsense-mediated decay.RNA biology · 2021Article
- Identification of a novel heterozygous mutation in the MITF gene in an Iranian family with Waardenburg syndrome type II using next-generation sequencing.Journal of clinical laboratory analysis · 2021Article
- Inappropriate cathepsin K secretion promotes its enzymatic activation driving heart and valve malformation.JCI insight · 2020Article
- Ribosome profiling at isoform level reveals evolutionary conserved impacts of differential splicing on the proteome.Nature communications · 2020Article
- Experimental supporting data on DIS3L2 over nonsense-mediated mRNA decay targets in human cells.Data in brief · 2020Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
mRNAs containing premature termination codons (PTCs) are rapidly degraded through nonsense-mediated mRNA decay (NMD). However, some PTC-containing mRNAs evade NMD, and might generate mutant proteins responsible for various diseases, including cancers. Using PTC-containing human genomic β-globin constructs, we show that a fraction (~30%) of PTC-containing mRNAs expressed from NMD-competent PTC-containing constructs were as stable as their PTC-free counterparts in a steady state. These PTC-containing mRNAs were monosome-enriched and rarely contributed to expression of mutant proteins. Expression of trace amounts of mutant proteins from NMD-competent PTC-containing constructs was not affected by inhibition of eIF4E-dependent translation and such expression was dependent on a continuous influx of newly synthesized PTC-containing mRNAs, indicating that truncated mutant proteins originated primarily in the pioneer round of translation. The generation of mutant proteins was promoted by UPF1 depletion, which induced polysome association of PTC-containing mRNAs, increased eIF4E-bound PTC-containing mRNA levels, and subsequent eIF4E-dependent translation. Our findings suggest that PTC-containing mRNAs are potent and regulatable sources of mutant protein generation.
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