ArticleGenes & development2014
A post-translational regulatory switch on UPF1 controls targeted mRNA degradation.
Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 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
124 citing papers in PubMed.
- A systems perspective on monoallelic inborn errors of immunity.Nature genetics · 2026Review
- Suppressor with morphogenetic effect on genitalia 7 (SMG7) drives hepatocellular carcinoma progression through context-dependent nonsense-mediated decay (NMD) dysregulation.Molecular biomedicine · 2026Article
- SMG1:SMG8:SMG9-complex integrity supports efficient execution of nonsense-mediated mRNA decay.Nucleic acids research · 2026Article
- Article
- Nonsense-mediated decay controls a negative feedback loop in innate immune sensing.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Nonsense-mediated mRNA decay and associated splicing patterns in neurodevelopmental disorders.Frontiers in molecular biosciences · 2026Review
- UPF1-dependent glycolysis driven by LINC00887 facilitates macrophage M2 polarization in clear cell renal cell carcinoma.Frontiers in immunology · 2026Article
- Pharmacologic inhibition of PCBP2 biomolecular condensates relieves Alzheimer's disease.Nature communications · 2025Article
- UPF1 shuttles between nucleus and cytoplasm independently of its RNA-binding and ATPase activities.RNA (New York, N.Y.) · 2025Article
- Nonsense-mediated mRNA decay: a key regulatory system engaged in cancer.Cell communication and signaling : CCS · 2025Review
- Cell-intrinsic regulation of HBV RNAs by the nonsense-mediated mRNA decay pathway controls viral replication.iScience · 2025Article
- Cell type- and factor-specific nonsense-mediated RNA decay.Nucleic acids research · 2025Article
- Bioinformatics-driven refinement of the commonly used TPI nonsense-mediated decay reporter system.RNA (New York, N.Y.) · 2024Article
- Modulation of UPF1 catalytic activity upon interaction of SARS-CoV-2 Nucleocapsid protein with factors involved in nonsense mediated-mRNA decay.Nucleic acids research · 2024Article
- Widespread 3'UTR capped RNAs derive from G-rich regions in proximity to AGO2 binding sites.BMC biology · 2024Article
- UPF1 plays critical roles in early B cell development.Nature communications · 2024Article
- UPF1 ATPase autoinhibition and activation modulate RNA binding kinetics and NMD efficiency.Nucleic acids research · 2024Article
- Physiological Consequences of Nonsense-Mediated Decay and Its Role in Adaptive Responses.Biomedicines · 2024Review
- UPF1 regulates mRNA stability by sensing poorly translated coding sequences.Cell reports · 2024Article
- Nonsense-mediated mRNA decay pathway in plants under stress: general gene regulatory mechanism and advances.Planta · 2024Review
64 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
7 authors.
Funding
Abstract
Nonsense-mediated mRNA decay (NMD) controls the quality of eukaryotic gene expression and also degrades physiologic mRNAs. How NMD targets are identified is incompletely understood. A central NMD factor is the ATP-dependent RNA helicase upframeshift 1 (UPF1). Neither the distance in space between the termination codon and the poly(A) tail nor the binding of steady-state, largely hypophosphorylated UPF1 is a discriminating marker of cellular NMD targets, unlike for premature termination codon (PTC)-containing reporter mRNAs when compared with their PTC-free counterparts. Here, we map phosphorylated UPF1 (p-UPF1)-binding sites using transcriptome-wide footprinting or DNA oligonucleotide-directed mRNA cleavage to report that p-UPF1 provides the first reliable cellular NMD target marker. p-UPF1 is enriched on NMD target 3' untranslated regions (UTRs) along with suppressor with morphogenic effect on genitalia 5 (SMG5) and SMG7 but not SMG1 or SMG6. Immunoprecipitations of UPF1 variants deficient in various aspects of the NMD process in parallel with Förster resonance energy transfer (FRET) experiments reveal that ATPase/helicase-deficient UPF1 manifests high levels of RNA binding and disregulated hyperphosphorylation, whereas wild-type UPF1 releases from nonspecific RNA interactions in an ATP hydrolysis-dependent mechanism until an NMD target is identified. 3' UTR-associated UPF1 undergoes regulated phosphorylation on NMD targets, providing a binding platform for mRNA degradative activities. p-UPF1 binding to NMD target 3' UTRs is stabilized by SMG5 and SMG7. Our results help to explain why steady-state UPF1 binding is not a marker for cellular NMD substrates and how this binding is transformed to induce mRNA decay.
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.