ArticleCell reports2024
Initiation of a ZAKα-dependent ribotoxic stress response by the innate immunity endoribonuclease RNase L.
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 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer.Molecular oncology · 2026Review
- The integrated stress response kinase GCN2 prevents ZAKα-Dependent inflammatory hyperactivation in macrophages.The Journal of biological chemistry · 2026Article
- PKR engages viral RNA and intron-retained host transcripts during poxvirus infection.Cell reports · 2026Article
- 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
- Integrated proteomic and transcriptomic profiles reveals the role of OAS3 in dermatomyositis pathogenesis.Frontiers in immunology · 2026Article
- Article
- 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
- 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
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
RNase L is an endoribonuclease of higher vertebrates that functions in antiviral innate immunity. Interferons induce oligoadenylate synthetase enzymes that sense double-stranded RNA of viral origin leading to the synthesis of 2',5'-oligoadenylate (2-5A) activators of RNase L. However, it is unknown precisely how RNase L remodels the host cell transcriptome. To isolate effects of RNase L from other effects of double-stranded RNA or virus, 2-5A is directly introduced into cells. Here, we report that RNase L activation by 2-5A causes a ribotoxic stress response involving the MAP kinase kinase kinase (MAP3K) ZAKα, MAP2Ks, and the stress-activated protein kinases JNK and p38α. RNase L activation profoundly alters the transcriptome by widespread depletion of mRNAs associated with different cellular functions but also by JNK/p38α-stimulated induction of inflammatory genes. These results show that the 2-5A/RNase L system triggers a protein kinase cascade leading to proinflammatory signaling and apoptosis.
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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.