ArticleNature communications2021
Identification of poly(ADP-ribose) polymerase 9 (PARP9) as a noncanonical sensor for RNA virus in dendritic cells.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.
- Bibliometric analysis of traditional Chinese medicine for viral infections through immune modulation (2015-2025).Frontiers in immunology · 2025Pooled it
- SKP2 Regulates Pulmonary Inflammatory Injury Triggered by Bacterial Infection Through p27-Mediated Degradation of FOXN3.MedComm · 2026Article
- Antiviral innate immunity in myocarditis: mechanisms and emerging therapeutics.Experimental & molecular medicine · 2026Review
- Mitochondrial RNA-Type I Interferon Axis in Sjögren's Disease: Molecular Mechanisms and Translational Implications.International journal of molecular sciences · 2026Review
- TRIM47 catalyzes MAVS SUMOylation to safeguard chronic viral infections and tissue inflammation.Cell communication and signaling : CCS · 2026Article
- NMR study of human macroPARPs domains:Biomolecular NMR assignments · 2026Article
- Decoding ulcerative colitis pathogenesis through transcriptomics: from dysregulated gene networks to targeted intervention strategies.Journal of translational autoimmunity · 2026Article
- CRISPR/Cas9-Mediated Knockout of CGNL1 Confers Resistance to Aflatoxin B1 in Porcine Intestinal Epithelial Cells via Suppressing ROS Generation.International journal of molecular sciences · 2026Article
- Transcriptomic Analysis of the Antiviral Responses in Ovine Type II Alveolar Epithelial Cells During Early Stage of Bluetongue Virus Infection.Animals : an open access journal from MDPI · 2026Article
- PARP1 stabilizes FOXN3 to suppress pulmonary fibrosis through p38-related feedback regulation.Science advances · 2026Article
- PARPs and PARP inhibitors: molecular mechanisms and clinical applications.Molecular biomedicine · 2025Review
- Interleukin-27 is antiviral against Zika virus at the maternal-fetal interface.Nature communications · 2025Article
- Global remodeling of ADP-ribosylation by PARP1 suppresses influenza A virus infection.Nature communications · 2025Article
- IRF3 in viral infections: more than just triggering the interferon response.Genes and immunity · 2025Review
- Review
- Regulation of antiviral and antimicrobial innate immunity and immune evasion.Cellular and molecular life sciences : CMLS · 2025Article
- Mono-ADP-ribosylating PARP enzymes in cellular signaling and disease.Journal of cell science · 2025Review
- Vertical transmission of Leishmania donovani with placental degeneration in the pregnant mouse model of visceral leishmaniasis.PLoS neglected tropical diseases · 2025Article
- Circovirus Rep evades immune restriction by disrupting cGAS oligomerization and phase separation.PLoS pathogens · 2025Article
- The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications.Signal transduction and targeted therapy · 2025Review
29 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
8 authors at 1 institution in 2 countries.
Funding
Abstract
Innate immune cells are critical in protective immunity against viral infections, involved in sensing foreign viral nucleic acids. Here we report that the poly(ADP-ribose) polymerase 9 (PARP9), a member of PARP family, serves as a non-canonical sensor for RNA virus to initiate and amplify type I interferon (IFN) production. We find knockdown or deletion of PARP9 in human or mouse dendritic cells and macrophages inhibits type I IFN production in response to double strand RNA stimulation or RNA virus infection. Furthermore, mice deficient for PARP9 show enhanced susceptibility to infections with RNA viruses because of the impaired type I IFN production. Mechanistically, we show that PARP9 recognizes and binds viral RNA, with resultant recruitment and activation of the phosphoinositide 3-kinase (PI3K) and AKT3 pathway, independent of mitochondrial antiviral-signaling (MAVS). PI3K/AKT3 then activates the IRF3 and IRF7 by phosphorylating IRF3 at Ser385 and IRF7 at Ser437/438 mediating type I IFN production. Together, we reveal a critical role for PARP9 as a non-canonical RNA sensor that depends on the PI3K/AKT3 pathway to produce type I IFN. These findings may have important clinical implications in controlling viral infections and viral-induced diseases by targeting PARP9.
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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.