ArticleJournal of virology2020
Severe Fever with Thrombocytopenia Syndrome Virus NSs Interacts with TRIM21 To Activate the p62-Keap1-Nrf2 Pathway.
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 37 papers.
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The trial behind it
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
- Interplay between SFTSV and host innate immunity: Viral evasion mechanisms, pathogenesis, and therapeutic perspectives.iScience · 2026Review
- TRIM21 is a molecular rheostat for influenza A virus replication.bioRxiv : the preprint server for biology · 2026Article
- Immune Cells at the Frontline of SFTSV Infection.Journal of microbiology and biotechnology · 2026Review
- Ferroptosis in veterinary medicine: mechanisms, therapies, and unmet challenges.The veterinary quarterly · 2025Review
- Article
- A viral necrosome mediates direct RIPK3 activation to promote inflammatory necroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- SFTSV NSs interacts with AGO2 to regulate the RNAi pathway for viral replication.Journal of virology · 2025Article
- Porcine reproductive and respiratory syndrome virus nsp5 inhibits the activation of the Nrf2/HO-1 pathway by targeting p62 to antagonize its antiviral activity.Journal of virology · 2025Article
- Verteporfin Inhibits Severe Fever with Thrombocytopenia Syndrome Virus Infection via Inducing the Degradation of the Viral Gn Protein.Pharmaceutics · 2025Article
- Advancements in vaccine development and therapeutic approaches for severe fever with Thrombocytopenia Syndrome.Frontiers in cellular and infection microbiology · 2025Review
- A Focus on the Mechanisms of Alteration in Host Lymphocyte Level Following Severe Fever with Thrombocytopenia Syndrome Virus (SFTSV) Infection.Journal of inflammation research · 2025Review
- Nrf2 Regulates Inflammation by Modulating Dendritic Cell-T Cell Crosstalk during Viral-Bacterial Superinfection.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Review
- Severe fever with thrombocytopenia syndrome virus induces lactylation of m6A reader protein YTHDF1 to facilitate viral replication.EMBO reports · 2024Article
- Review
- TRIM21 Promotes Oxidative Stress and Ferroptosis through the SQSTM1-NRF2-KEAP1 Axis to Increase the Titers of H5N1 Highly Pathogenic Avian Influenza Virus.International journal of molecular sciences · 2024Article
- Current Progress of Severe Fever with Thrombocytopenia Syndrome Virus (SFTSV) Vaccine Development.Viruses · 2024Review
- The Role of the NRF2 Pathway in the Pathogenesis of Viral Respiratory Infections.Pathogens (Basel, Switzerland) · 2023Review
- Dysregulation of intracellular redox homeostasis by the SARS-CoV-2 ORF6 protein.Virology journal · 2023Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Nuclear factor erythroid 2-related factor 2 (Nrf2) dissociates from its inhibitor, Keap1, upon stress signals and subsequently induces an antioxidant response that critically controls the viral life cycle and pathogenesis. Besides intracellular Fc receptor function, tripartite motif 21 (TRIM21) E3 ligase plays an essential role in the p62-Keap1-Nrf2 axis pathway for redox homeostasis. Specifically, TRIM21-mediated p62 ubiquitination abrogates p62 oligomerization and sequestration activity and negatively regulates the Keap1-Nrf2-mediated antioxidant response. A number of viruses target the Nrf2-mediated antioxidant response to generate an optimal environment for their life cycle. Here we report that a nonstructural protein (NSs) of severe fever with thrombocytopenia syndrome virus (SFTSV) interacts with and inhibits TRIM21 to activate the Nrf2 antioxidant signal pathway. Mass spectrometry identified TRIM21 to be a binding protein for NSs. NSs bound to the carboxyl-terminal SPRY subdomain of TRIM21, enhancing p62 stability and oligomerization. This facilitated p62-mediated Keap1 sequestration and ultimately increased Nrf2-mediated transcriptional activation of antioxidant genes, including those for heme oxygenase 1, NAD(P)H quinone oxidoreductase 1, and CD36. Mutational analysis found that the NSs-A46 mutant, which no longer interacted with TRIM21, was unable to increase Nrf2-mediated transcriptional activation. Functionally, the NS wild type (WT), but not the NSs-A46 mutant, increased the surface expression of the CD36 scavenger receptor, resulting in an increase in phagocytosis and lipid uptake. A combination of reverse genetics and assays with
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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.