ArticlePloS one2016
Alteration of Antiviral Signalling by Single Nucleotide Polymorphisms (SNPs) of Mitochondrial Antiviral Signalling Protein (MAVS).
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Genome-wide association study identifies and validates genetic variation in the RIG-I/MAVS signaling pathway associated with HIV-related Kaposi sarcoma in children and adults.Frontiers in oncology · 2026Article
- MAVS signaling is required for preventing persistent chikungunya heart infection and chronic vascular tissue inflammation.Nature communications · 2023Article
- PSnpBind-ML: predicting the effect of binding site mutations on protein-ligand binding affinity.Journal of cheminformatics · 2023Article
- MAVS Expression in Alveolar Macrophages Is Essential for Host Resistance againstJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- The MAVS Immune Recognition Pathway in Viral Infection and Sepsis.Antioxidants & redox signaling · 2021Review
- Modeling the complete kinetics of coxsackievirus B3 reveals human determinants of host-cell feedback.Cell systems · 2021Article
- Review
- lncRNASNP2: an updated database of functional SNPs and mutations in human and mouse lncRNAs.Nucleic acids research · 2018Article
- Bone Marrow-Derived Mesenchymal Stem Cells From Patients With Systemic Lupus Erythematosus Have a Senescence-Associated Secretory Phenotype Mediated by a Mitochondrial Antiviral Signaling Protein-Interferon-β Feedback Loop.Arthritis & rheumatology (Hoboken, N.J.) · 2017Article
- The Absence of Interferon-β Promotor Stimulator-1 (IPS-1) Predisposes to Bronchiolitis and Asthma-like Pathology in Response to Pneumoviral Infection in Mice.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic variation is associated with diseases. As a type of genetic variation occurring with certain regularity and frequency, the single nucleotide polymorphism (SNP) is attracting more and more attention because of its great value for research and real-life application. Mitochondrial antiviral signalling protein (MAVS) acts as a common adaptor molecule for retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), which can recognize foreign RNA, including viral RNA, leading to the induction of type I interferons (IFNs). Therefore, MAVS is thought to be a crucial molecule in antiviral innate immunity. We speculated that genetic variation of MAVS may result in susceptibility to infectious diseases. To assess the risk of viral infection based on MAVS variation, we tested the effects of twelve non-synonymous MAVS coding-region SNPs from the National Center for Biotechnology Information (NCBI) database that result in amino acid substitutions. We found that five of these SNPs exhibited functional alterations. Additionally, four resulted in an inhibitory immune response, and one had the opposite effect. In total, 1,032 human genomic samples obtained from a mass examination were genotyped at these five SNPs. However, no homozygous or heterozygous variation was detected. We hypothesized that these five SNPs are not present in the Japanese population and that such MAVS variations may result in serious immune diseases.
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