ArticleThe EMBO journal1996
A splicing-dependent regulatory mechanism that detects translation signals.
Article in The EMBO journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
114 citing papers in PubMed, 273 citations in OpenAlex.
- The position of premature termination codons in the hepatocyte nuclear factor -1 beta gene determines susceptibility to nonsense-mediated decay.Human genetics · 2005Trial
- Real-time imaging of transcriptional feedback in nonsense-mediated mRNA decay.Science advances · 2026Article
- Beyond quality control: biological roles of nonsense-mediated RNA decay.The EMBO journal · 2026Review
- Molecular Consequences ofInternational journal of molecular sciences · 2025Article
- Bioinformatics-driven refinement of the commonly used TPI nonsense-mediated decay reporter system.RNA (New York, N.Y.) · 2024Article
- Physiological Consequences of Nonsense-Mediated Decay and Its Role in Adaptive Responses.Biomedicines · 2024Review
- Characterization of the mIF4G Domains in the RNA Surveillance Protein Upf2p.Current issues in molecular biology · 2023Article
- Enhanced nuclear translation is associated with proliferation and progression across multiple cancers.MedComm · 2023Article
- Inhibition of Nonsense-Mediated Decay Induces Nociceptive Sensitization through Activation of the Integrated Stress Response.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Nonsense-mediated mRNA decay uses complementary mechanisms to suppress mRNA and protein accumulation.Life science alliance · 2022Article
- Validation of DE50-MD dogs as a model for the brain phenotype of Duchenne muscular dystrophy.Disease models & mechanisms · 2022Article
- Molecular Determinants and Specificity of mRNA with Alternatively-Spliced UPF1 Isoforms, Influenced by an Insertion in the 'Regulatory Loop'.International journal of molecular sciences · 2021Article
- Evidence in disease and non-disease contexts that nonsense mutations cause altered splicing via motif disruption.Nucleic acids research · 2021Article
- Nonsense-Mediated RNA Decay Is a Unique Vulnerability of Cancer Cells HarboringCancer research · 2021Article
- Perspective in Alternative Splicing Coupled to Nonsense-Mediated mRNA Decay.International journal of molecular sciences · 2020Review
- Article
- UPF1-Mediated RNA Decay-Danse Macabre in a Cloud.Biomolecules · 2020Review
- How to get away with nonsense: Mechanisms and consequences of escape from nonsense-mediated RNA decay.Wiley interdisciplinary reviews. RNA · 2020Review
- Nonsense-mediated mRNA decay efficiency varies in choroideremia providing a target to boost small molecule therapeutics.Human molecular genetics · 2019Article
- Aberrant splicing in B-cell acute lymphoblastic leukemia.Nucleic acids research · 2018Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Premature termination codons (PTCs) can cause the decay of mRNAs in the nuclear fraction of mammalian cells. This enigmatic nuclear response is of interest because it suggests that translation signals do not restrict their effect to the cytoplasm, where fully assembled ribosomes reside. Here we examined the molecular mechanism for this putative nuclear response by using the T-cell receptor-beta (TCR-beta) gene, which acquires PTCs as a result of programmed rearrangements that occur during normal thymic ontogeny. We found that PTCs had little or no measurable effect on TCR-beta pre-mRNA levels, but they sharply depressed TCR-beta mature mRNA levels in the nuclear fraction of stably transfected cells. A PTC split by an intron was able to trigger the down-regulatory response, implying that PTC recognition occurs after an mRNA is at least partially spliced. However, intron deletion and addition studies demonstrated that a PTC must be followed by at least one functional (spliceable) intron to depress mRNA levels. One explanation for this downstream intron-dependence is that cytoplasmic ribosomes adjacent to nuclear pores scan mRNAs still undergoing splicing as they emerge from the nucleus. We found this explanation to be unlikely because PTCs only 8 or 10 nt upstream of a terminal intron down-regulated mRNA levels, even though this distance is too short to permit PTC recognition in the cytoplasm prior to the splicing of the downstream intron in the nucleus. Collectively, the results suggest that nonsense codon recognition may occur in the nucleus.
Indexed as
Identifiers
8918474PMC452383W1268830682What OpenQuestion holds
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.