ArticleRNA (New York, N.Y.)2017
Inhibition of nonsense-mediated RNA decay by ER stress.
Article in RNA (New York, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 67 citations in OpenAlex.
- RBM39 modulates UPR signaling through alternative splicing of IRE1α/Genes & development · 2026Article
- TDP-43 promotes allergen-induced inflammation and influenza A virus replication in airway epithelium.Nature communications · 2026Article
- PERK orchestrates an endoplasmic reticulum stress alternative splicing program via CLK1/SRSF1.Nature communications · 2026Article
- The nonsense-mediated decay RNA-surveillance pathway facilitates the hypoxia response bybioRxiv : the preprint server for biology · 2026Article
- TDP43 and hnRNP K Regulate Alternative Splicing of DNAJC5.Cell biology international · 2026Article
- The implications of alternative splicing regulation for maximum lifespan.Nature communications · 2025Article
- The Implications of Alternative Splicing Regulation for Maximum Lifespan.bioRxiv : the preprint server for biology · 2025Article
- Optogenetic Clustering of Human IRE1 Reveals Differential Regulation of Transcription and mRNA Splice Isoform Abundance by the UPR.bioRxiv : the preprint server for biology · 2025Article
- Messenger RNA Surveillance: Current Understanding, Regulatory Mechanisms, and Future Implications.Molecular biotechnology · 2025Review
- A WFS1 variant disrupting acceptor splice site uncovers the impact of alternative splicing on beta cell apoptosis in a patient with Wolfram syndrome.Diabetologia · 2025Article
- Nonsense-Mediated mRNA Decay: Mechanistic Insights and Physiological Significance.Molecular biotechnology · 2024Review
- Disrupted Post-Transcriptional Regulation of Gene Expression as a Hallmark of Fatty Liver Progression.International journal of molecular sciences · 2024Article
- The Art of Finding the Right Drug Target: Emerging Methods and Strategies.Pharmacological reviews · 2024Review
- UPF3B modulates endoplasmic reticulum stress through interaction with inositol-requiring enzyme-1α.Cell death & disease · 2024Article
- Epistatic interactions between NMD and TRP53 control progenitor cell maintenance and brain size.Neuron · 2024Article
- CellTICS: an explainable neural network for cell-type identification and interpretation based on single-cell RNA-seq data.Briefings in bioinformatics · 2023Article
- Mapping genetic variants for nonsense-mediated mRNA decay regulation across human tissues.Genome biology · 2023Article
- Compromised nonsense-mediated RNA decay results in truncated RNA-binding protein production upon DUX4 expression.Cell reports · 2023Article
- Characterization of a rhabdomyosarcoma reveals a critical role for SMG7 in cancer cell viability and tumor growth.Scientific reports · 2023Article
- Nonsense-mediated mRNA decay promote C2C12 cell proliferation by targeting PIK3R5.Journal of muscle research and cell motility · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Nonsense-mediated RNA decay (NMD) selectively degrades mutated and aberrantly processed transcripts that contain premature termination codons (PTC). Cellular NMD activity is typically assessed using exogenous PTC-containing reporters. We overcame some inherently problematic aspects of assaying endogenous targets and developed a broadly applicable strategy to reliably and easily monitor changes in cellular NMD activity. Our new method was genetically validated for distinguishing NMD regulation from transcriptional control and alternative splicing regulation, and unexpectedly disclosed a different sensitivity of NMD targets to NMD inhibition. Applying this robust method for screening, we identified NMD-inhibiting stressors but also found that NMD inactivation was not universal to cellular stresses. The high sensitivity and broad dynamic range of our method revealed a strong correlation between NMD inhibition, endoplasmic reticulum (ER) stress, and polysome disassembly upon thapsigargin treatment in a temporal and dose-dependent manner. We found little evidence of calcium signaling mediating thapsigargin-induced NMD inhibition. Instead, we discovered that of the three unfolded protein response (UPR) pathways activated by thapsigargin, mainly protein kinase RNA-like endoplasmic reticulum kinase (PERK) was required for NMD inhibition. Finally, we showed that ER stress compounded TDP-43 depletion in the up-regulation of NMD isoforms that had been implicated in the pathogenic mechanisms of amyotrophic lateral sclerosis and frontotemporal dementia, and that the additive effect of ER stress was completely blocked by PERK deficiency.
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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.