ArticleJournal of virology2020
VAMP8 Contributes to the TRIM6-Mediated Type I Interferon Antiviral Response during West Nile Virus Infection.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Differential Interactions of Tissue-Restricted Host Proteins SPLUNC1 and VAMP8 with VP3 of Human Bocaviruses 1 and 2.Pathogens (Basel, Switzerland) · 2026Article
- VAMP8 function reveals tight linkage between endocytic recycling and endocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Immune cell-resolved transcriptomics provides insights into the basis for variations of fish genetic resistance to viral disease.BMC biology · 2025Article
- Seneca Valley virus 3C protease targets TRIM32 for cleavage to antagonize its antiviral effects.Journal of virology · 2025Article
- A No-Brainer! The Therapeutic Potential of TRIM Proteins in Viral and Central Nervous System Diseases.Viruses · 2025Review
- TRIM6 Promotes Cell Cycle and Growth by Modulating p53 Signaling Pathway in Lung Adenocarcinoma.International journal of general medicine · 2025Article
- TRIMming down Flavivirus Infections.Viruses · 2024Review
- Vesicle-associated membrane protein 8 knockdown exerts anti-proliferative, pro-apoptotic, anti-autophagic, and pro-ferroptotic effects on colorectal cancer cells by inhibition of the JAK/STAT3 pathway.Journal of bioenergetics and biomembranes · 2024Article
- Early cellular and molecular signatures correlate with severity of West Nile virus infection.iScience · 2023Article
- The Molecular and Function Characterization of Porcine MID2.Animals : an open access journal from MDPI · 2023Article
- Hepatocyte CD36 modulates UBQLN1-mediated proteasomal degradation of autophagic SNARE proteins contributing to septic liver injury.Autophagy · 2023Article
- TRIM6: An Upregulated Biomarker with Prognostic Significance and Immune Correlations in Gliomas.Biomolecules · 2023Article
- The Role of Ubiquitin-Proteasome System in the Pathogenesis of Severe Acute Respiratory Syndrome Coronavirus-2 Disease.International journal of inflammation · 2023Review
- Molecular pathogenesis of Japanese encephalitis and possible therapeutic strategies.Archives of virology · 2022Review
- The RNA helicase DHX16 recognizes specific viral RNA to trigger RIG-I-dependent innate antiviral immunity.Cell reports · 2022Article
- Tyrphostin AG1024 Suppresses Coronaviral Replication by Downregulating JAK1 via an IR/IGF-1R Independent Proteolysis Mediated by Ndfip1/2_NEDD4-like E3 Ligase Itch.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Regulation of cGAS/STING signaling and corresponding immune escape strategies of viruses.Frontiers in cellular and infection microbiology · 2022Review
- Flaviviruses: Innate Immunity, Inflammasome Activation, Inflammatory Cell Death, and Cytokines.Frontiers in immunology · 2022Review
- Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Several members of the tripartite motif (TRIM) family of E3 ubiquitin ligases regulate immune pathways, including the antiviral type I interferon (IFN-I) system. Previously, we demonstrated that TRIM6 is involved in IFN-I induction and signaling. In the absence of TRIM6, optimal IFN-I signaling is reduced, allowing increased replication of interferon-sensitive viruses. Despite having evolved numerous mechanisms to restrict the vertebrate host's IFN-I response, West Nile virus (WNV) replication is sensitive to pretreatment with IFN-I. However, the regulators and products of the IFN-I pathway that are important in regulating WNV replication are incompletely defined. Consistent with WNV's sensitivity to IFN-I, we found that in TRIM6 knockout (TRIM6-KO) A549 cells, WNV replication is significantly increased and IFN-I induction and signaling are impaired compared to wild-type (wt) cells. IFN-β pretreatment was more effective in protecting against subsequent WNV infection in wt cells than TRIM6-KO, indicating that TRIM6 contributes to the establishment of an IFN-induced antiviral response against WNV. Using next-generation sequencing, we identified VAMP8 as a potential factor involved in this TRIM6-mediated antiviral response. VAMP8 knockdown resulted in reduced JAK1 and STAT1 phosphorylation and impaired induction of several interferon-stimulated genes (ISGs) following WNV infection or IFN-β treatment. Furthermore, VAMP8-mediated STAT1 phosphorylation required the presence of TRIM6. Therefore, the VAMP8 protein is a novel regulator of IFN-I signaling, and its expression and function are dependent on TRIM6 activity. Overall, these results provide evidence that TRIM6 contributes to the antiviral response against WNV and identify VAMP8 as a novel regulator of the IFN-I system.
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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.