ArticleScience advances2025
Effective recognition of double-stranded RNA does not require activation of cellular inflammation.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Cold-adapted RNA polymerase fromProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Sub-stoichiometric 5-methoxyuridine modification enables tunable immune evasion and protein expression from synthetic mRNAs.Molecular therapy. Nucleic acids · 2026Article
- An Ultrastructural and Proteomic Analysis in DM1 Young Adults' Myoblasts: Stressed RER and Mitochondrial Dysfunction Involvement.Journal of cellular and molecular medicine · 2026Article
- Uridine analogs prevent stress granule formation, not by blocking PKR recognition, but by inhibiting the synthesis of T7 RNA polymerase byproducts.RNA (New York, N.Y.) · 2026Article
- Sensing of double-stranded RNA in human cells: molecular mechanisms and cellular consequences.Biochemical Society transactions · 2026Review
- PUS1 Drives Renal Cancer Progression by Preventing Formation of Endogenous Double-stranded RNAs.International journal of biological sciences · 2026Article
- Emerging Technologies Tackling Adeno-Associated Viruses (AAV) Immunogenicity in Gene Therapy Applications.Pharmaceutics · 2025Review
- Exploring the Impact of In Vitro-Transcribed mRNA Impurities on Cellular Responses.Analytical chemistry · 2024Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excess double-stranded RNA (dsRNA) is present in the cytoplasm of human cells, usually following viral infections. Recognition of dsRNAs activates innate immune pathways, leading to cellular inflammation and inhibition of cell growth. Here, we show that an effective dsRNA response may occur without the onset of inflammation. Pro-inflammatory [RLR (retinoic acid-inducible gene I-like receptor)-dependent pathway] and cell growth inhibitory mechanisms [oligoadenylate synthetase (OAS)/ribonuclease L (RNase L)- and dsRNA-activated protein kinase (PKR)-dependent pathways] can act independently. We found that the 5' ends of dsRNA direct the onset of cellular inflammation, whereas the RNA duplex activates the OAS/RNase L and PKR pathways. Unexpectedly, three of the most common human RNA epitranscriptomic marks-i.e.,
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Registered trials
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