ArticleCell cycle (Georgetown, Tex.)2016
Foot-and-mouth disease virus structural protein VP3 degrades Janus kinase 1 to inhibit IFN-γ signal transduction pathways.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 52 citations in OpenAlex.
- Encephalomyocarditis virus evades IFN-mediated antiviral response by RNF149 targeting JAK1 for ubiquitination and degradation.Virulence · 2026Article
- Review
- STING1 negatively regulates translation and replication of foot-and-mouth disease virus independently of interferon and is antagonized by the viral proteins 3C and 2B.Virologica Sinica · 2026Article
- FMDV VP3 Induces IL-10 Expression in Porcine Macrophages via PI3K Interaction and PI3K/AKT-mTOR Pathway Activation.Viruses · 2026Article
- Article
- MARCH8 promotes the proteasomal degradation of foot-and-mouth disease virus VP1, VP2, and VP3 to negatively regulate viral replication.Veterinary research · 2025Article
- Foot-and-mouth disease: genomic and proteomic structure, antigenic sites, serotype relationships, immune evasion, recent vaccine development strategies, and future perspectives.Veterinary research · 2025Review
- Foot-and-mouth disease in Asia.Virus research · 2025Review
- Foot-and-mouth disease virus (FMDV) negatively regulates ZFP36 protein expression to alleviate its antiviral activity.Journal of virology · 2024Article
- Picornavirus VP3 protein induces autophagy through the TP53-BAD-BAX axis to promote viral replication.Autophagy · 2024Article
- Article
- 3CVirologica Sinica · 2023Article
- EHBP1L1 Drives Immune Evasion in Renal Cell Carcinoma through Binding and Stabilizing JAK1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The influenza virus PB2 protein evades antiviral innate immunity by inhibiting JAK1/STAT signalling.Nature communications · 2022Article
- Foot-and-Mouth Disease Virus: Molecular Interplays with IFN Response and the Importance of the Model.Viruses · 2022Review
- Foot-and-mouth disease virus non-structural protein 2B downregulates the RLR signaling pathwayFrontiers in immunology · 2022Article
- Expression Profiles of Differentially Expressed Circular RNAs and circRNA-miRNA-mRNA Regulatory Networks in SH-SY5Y Cells Infected with Coxsackievirus B5.International journal of genomics · 2022Article
- A defective viral genome strategy elicits broad protective immunity against respiratory viruses.Cell · 2021Article
- Foot-and-Mouth Disease Virus VP3 Protein Acts as a Critical Proinflammatory Factor by Promoting Toll-Like Receptor 4-Mediated Signaling.Journal of virology · 2021Article
- Inhibition of MAVS Aggregation-Mediated Type-I Interferon Signaling by Foot-and-Mouth Disease Virus VP3.Viruses · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Foot-and-mouth disease is a highly contagious viral disease of cloven-hoofed animals that is caused by foot-and-mouth disease virus (FMDV). To replicate efficiently in vivo, FMDV has evolved methods to circumvent host antiviral defense mechanisms, including those induced by interferons (IFNs). Previous research has focused on the effect of FMDV L(pro) and 3C(pro) on type I IFNs. In this study, FMDV VP3 was found to inhibit type II IFN signaling pathways. The overexpression of FMDV VP3 inhibited the IFN-γ-triggered phosphorylation of STAT1 at Tyr701 and the subsequent expression of downstream genes. Mechanistically, FMDV VP3 interacted with JAK1/2 and inhibited the tyrosine phosphorylation, dimerization and nuclear accumulation of STAT1. FMDV VP3 also disrupted the assembly of the JAK1 complex and degraded JAK1 but not JAK2 via a lysosomal pathway. Taken together, the results reveal a novel mechanism used by which FMDV VP3 counteracts the type II IFN signaling pathways.
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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.