ArticleCell reports2024
Endonucleolytic RNA cleavage drives changes in gene expression during the innate immune response.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed.
- Mechanism of RACK1-dependent ZAKα activation at stalled and collided ribosomes.Molecular cell · 2026Article
- Stalled translation on transcripts cleaved by RNase L activates signaling important for innate immunity.RNA (New York, N.Y.) · 2026Article
- Article
- Cytoplasmic mRNA decay by the antiviral nuclease RNase L promotes transcriptional repression.Cell reports · 2026Article
- RNase L regulates the antiviral proteome by accelerating mRNA decay, inhibiting nuclear mRNA export, and repressing transcription.Cell reports · 2026Article
- RNase L Regulates Antiviral Responsiveness through Cleavage of XBP1 mRNA.bioRxiv : the preprint server for biology · 2026Article
- 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
- Cell cycle regulation by the ribotoxic stress response.Trends in cell biology · 2025Review
- Stalled translation on transcripts cleaved by RNase L activates signaling important for innate immunity.bioRxiv : the preprint server for biology · 2025Article
- Cooperative role of PACT and ADAR1 in preventing aberrant PKR activation by self-derived double-stranded RNA.Nature communications · 2025Article
- Regulating Immune Responses Induced by PEGylated Messenger RNA-Lipid Nanoparticle Vaccine.Vaccines · 2024Review
- DHX15 and Rig-I Coordinate Apoptosis and Innate Immune Signaling by Antiviral RNase L.Viruses · 2024Article
- The Unusual Role of Ribonuclease L in Innate Immunity.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Viral infection triggers several double-stranded RNA (dsRNA) sensors that lead to changes in gene expression in the cell. One of these sensors activates an endonuclease, ribonuclease L (RNase L), that cleaves single-stranded RNA. However, how the resultant widespread RNA fragmentation affects gene expression is not fully understood. Here, we show that this fragmentation induces the ribotoxic stress response via ZAKα, potentially through stalled ribosomes and/or ribosome collisions. The p38 and JNK pathways that are activated as part of this response promote outcomes that inhibit the virus, such as programmed cell death. We also show that RNase L limits the translation of stress-responsive genes. Intriguingly, we found that the activity of the generic endonuclease, RNase A, recapitulates many of the same molecular phenotypes as activated RNase L, demonstrating how widespread RNA cleavage can evoke an antiviral program.
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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.