ArticleCell2016
The Antagonistic Gene Paralogs Upf3a and Upf3b Govern Nonsense-Mediated RNA Decay.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
106 citing papers in PubMed, 165 citations in OpenAlex.
- Beyond quality control: biological roles of nonsense-mediated RNA decay.The EMBO journal · 2026Review
- Article
- The nonsense-mediated mRNA decay factor Upf3 negatively regulates bulk autophagy progression inAutophagy reports · 2026Article
- Gene regulation through exon junction complex modularity.Nature structural & molecular biology · 2025Review
- Synergistic Methods to Investigate Eukaryotic Translation and Its Quality Control.Journal of molecular biology · 2025Review
- RANBP9 and RANBP10 cooperate in regulating non-small cell lung cancer proliferation.Journal of experimental & clinical cancer research : CR · 2025Article
- Nonsense-Mediated mRNA Decay: Mechanisms and Recent Implications in Cardiovascular Diseases.Cells · 2025Review
- Biological roles of nonsense-mediated RNA decay: insights from the nervous system.Current opinion in genetics & development · 2025Review
- Opposing roles of pseudokinases NRBP1 and NRBP2 in regulating L1 retrotransposition.Nature communications · 2025Article
- Cell type- and factor-specific nonsense-mediated RNA decay.Nucleic acids research · 2025Article
- Genetic and functional analysis of unproductive splicing using LeafCutter2.bioRxiv : the preprint server for biology · 2025Article
- Messenger RNA Surveillance: Current Understanding, Regulatory Mechanisms, and Future Implications.Molecular biotechnology · 2025Review
- HnRNPR-mediated UPF3B mRNA splicing drives hepatocellular carcinoma metastasis.Journal of advanced research · 2025Article
- The Intricate Functional Networks of Pre-mRNA Alternative Splicing in Mammalian Spermatogenesis.International journal of molecular sciences · 2024Review
- Nonsense-Mediated mRNA Decay: Mechanistic Insights and Physiological Significance.Molecular biotechnology · 2024Review
- Whole exome sequencing analysis of 167 men with primary infertility.BMC medical genomics · 2024Article
- RNA Surveillance Factor SMG5 Is Essential for Mouse Embryonic Stem Cell Differentiation.Biomolecules · 2024Article
- Epistatic interactions between NMD and TRP53 control progenitor cell maintenance and brain size.Neuron · 2024Article
- Article
- Proinflammatory Cytokines Suppress Nonsense-Mediated RNA Decay to Impair Regulated Transcript Isoform Processing in Pancreatic β-Cells.bioRxiv : the preprint server for biology · 2024Article
46 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
Gene duplication is a major evolutionary force driving adaptation and speciation, as it allows for the acquisition of new functions and can augment or diversify existing functions. Here, we report a gene duplication event that yielded another outcome--the generation of antagonistic functions. One product of this duplication event--UPF3B--is critical for the nonsense-mediated RNA decay (NMD) pathway, while its autosomal counterpart--UPF3A--encodes an enigmatic protein previously shown to have trace NMD activity. Using loss-of-function approaches in vitro and in vivo, we discovered that UPF3A acts primarily as a potent NMD inhibitor that stabilizes hundreds of transcripts. Evidence suggests that UPF3A acquired repressor activity through simple impairment of a critical domain, a rapid mechanism that may have been widely used in evolution. Mice conditionally lacking UPF3A exhibit "hyper" NMD and display defects in embryogenesis and gametogenesis. Our results support a model in which UPF3A serves as a molecular rheostat that directs developmental events.
Indexed as
Identifiers
What 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.