ReviewFrontiers in immunology2016
Accessory Factors of Cytoplasmic Viral RNA Sensors Required for Antiviral Innate Immune Response.
Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- Structural and functional perspectives on DEAD-box RNA helicases in the rubber tree cold stress response.Frontiers in plant science · 2026Review
- Identification and coregulation pattern analysis of long noncoding RNAs in the mouse brain after Angiostrongylus cantonensis infection.Parasites & vectors · 2024Article
- Two Modes of Th1 Polarization Induced by Dendritic-Cell-Priming Adjuvant in Vaccination.Cells · 2023Review
- IFN-Induced PARPs-Sensors of Foreign Nucleic Acids?Pathogens (Basel, Switzerland) · 2023Review
- Melatonin: Regulation of Viral Phase Separation and Epitranscriptomics in Post-Acute Sequelae of COVID-19.International journal of molecular sciences · 2022Review
- Human Beta Papillomavirus Type 8 E1 and E2 Proteins Suppress the Activation of the RIG-I-Like Receptor MDA5.Viruses · 2022Article
- Predicting diagnostic gene expression profiles associated with immune infiltration in patients with lupus nephritis.Frontiers in immunology · 2022Article
- The lncRNAs involved in regulating the RIG-I signaling pathway.Frontiers in cellular and infection microbiology · 2022Review
- Virus-Induced Tumorigenesis and IFN System.Biology · 2021Review
- Review
- To "Z" or not to "Z": Z-RNA, self-recognition, and the MDA5 helicase.PLoS genetics · 2021Review
- Type I and III IFN-mediated antiviral actions counteracted by SARS-CoV-2 proteins and host inherited factors.Cytokine & growth factor reviews · 2021Review
- Identification and Validation of IFI44 as Key Biomarker in Lupus Nephritis.Frontiers in medicine · 2021Article
- Regulation of Antiviral Immune Response byFrontiers in microbiology · 2021Review
- Analysis of Porcine RIG-I Like Receptors Revealed the Positive Regulation of RIG-I and MDA5 by LGP2.Frontiers in immunology · 2021Article
- Article
- A mathematic model to reveal delicate cross-regulation between MAVS/STING, inflammasome and MyD88-dependent type I interferon signalling.Journal of cellular and molecular medicine · 2020Article
- Immune Sensing Mechanisms that Discriminate Self from Altered Self and Foreign Nucleic Acids.Immunity · 2020Review
- Assessment of Prolonged Dengue Virus Infection in Dermal Fibroblasts and Hair-Follicle Dermal Papilla Cells.Viruses · 2020Article
- Mitochondrial Interactome: A Focus on Antiviral Signaling Pathways.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I interferon (IFN) induces many antiviral factors in host cells. RIG-I-like receptors (RLRs) are cytoplasmic viral RNA sensors that trigger the signal to induce the innate immune response that includes type I IFN production. RIG-I and MDA5 are RLRs that form nucleoprotein filaments along viral double-stranded RNA, resulting in the activation of MAVS adaptor molecule. The MAVS protein forms a prion-like aggregation structure, leading to type I IFN production. RIG-I and MDA5 undergo post-translational modification. TRIM25 and Riplet ubiquitin ligases deliver a K63-linked polyubiquitin moiety to the RIG-I N-terminal caspase activation and recruitment domains (CARDs) and C-terminal region; the polyubiquitin chain then stabilizes the two-CARD tetramer structure required for MAVS assembly. MDA5 activation is regulated by phosphorylation. RIOK3 is a protein kinase that phosphorylates the MDA5 protein in a steady state, and PP1α/γ dephosphorylate this protein, resulting in its activation. RIG-I and MDA5 require cytoplasmic RNA helicases for their efficient activation. LGP2, another RLR, is an RNA helicase involved in RLR signaling. This protein does not possess N-terminal CARDs and, thus, cannot trigger downstream signaling by itself. Recent studies have revealed that this protein modulates MDA5 filament formation, resulting in enhanced type I IFN production. Several other cytoplasmic RNA helicases are involved in RLR signaling. DDX3, DHX29, DHX36, and DDX60 RNA helicases have been reported to be involved in RLR-mediated type I IFN production after viral infection. However, the underlying mechanism is largely unknown. Future studies are required to reveal the role of RNA helicases in the RLR signaling pathway.
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