ArticleJournal of virology2014
Enterovirus 71 3C inhibits cytokine expression through cleavage of the TAK1/TAB1/TAB2/TAB3 complex.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
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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.
The trial behind it
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
71 citing papers in PubMed, 96 citations in OpenAlex.
- PANoptosis in the pathogenesis of myelodysplastic syndromes.Molecular oncology · 2026Review
- LncRNA-MSTRG.16919.1 regulates the proliferation of BHV-1 in MDBK cells through TAK1/TAB1/TAB2/TAB3 complexes.BMC veterinary research · 2026Article
- RNF31 restricts EV-A71 replication through innate immune activation and VP4 degradation, and is antagonized by viral 3C proteases.PLoS pathogens · 2026Article
- Coxsackievirus B3 Cleaves INTS10 Through 3C Protease to Facilitate Its Replication.International journal of molecular sciences · 2026Article
- Gene Therapy with Enterovirus 3 C Protease: A Promising Strategy for Various Solid Tumors.Nature communications · 2025Article
- Insight into the Life Cycle of Enterovirus-A71.Viruses · 2025Review
- The strategies and mechanisms of enteroviruses to evade innate immunity and the vaccine progress of enteroviruses.Frontiers in cellular and infection microbiology · 2025Review
- Cleavage of Stau2 by 3C protease promotes EV-A71 replication.Virology journal · 2024Article
- Recent Progress in Innate Immune Responses to Enterovirus A71 and Viral Evasion Strategies.International journal of molecular sciences · 2024Review
- TLR4 signalling: the key to controlling EV71 replication and inflammatory response.Frontiers in cellular and infection microbiology · 2024Article
- Versatility of the Zinc-Finger Antiviral Protein (ZAP) As a Modulator of Viral Infections.International journal of biological sciences · 2024Review
- Review
- Research progress on pathogenic and therapeutic mechanisms of Enterovirus A71.Archives of virology · 2023Review
- TRAF3 activates STING-mediated suppression of EV-A71 and target of viral evasion.Signal transduction and targeted therapy · 2023Article
- Mechanism of regulating macrophages/osteoclasts in attenuating wear particle-induced aseptic osteolysis.Frontiers in immunology · 2023Review
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
- Review
- H5N1 infection impairs the alveolar epithelial barrier through intercellular junction proteins via Itch-mediated proteasomal degradation.Communications biology · 2022Article
- Article
- Pharmacological perturbation of CXCL1 signaling alleviates neuropathogenesis in a model of HEVA71 infection.Nature communications · 2022Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
unlabelledEnterovirus 71 (EV71) causes hand, foot, and mouth disease in young children and infants. Severe infection with EV71 can lead to various neurological complications or fatal diseases. However, the mechanism of EV71 pathogenesis is poorly understood. Emerging evidence suggests that EV71 modulates type I interferon (IFN) and cytokine responses. Here, we show that EV71 disables components of the TAB2 complex through the 3C protein. When expressed in mammalian cells, EV71 3C interacts with TAB2 and TAK1, which inhibits NF-κB activation. Furthermore, 3C mediates cleavage of TAB2 and its partners, which requires the protease activity. H40D or C147S substitution in the 3C active sites abolishes its activity, whereas R84Q or V154S substitution in the RNA binding domain has no effect. The 3C protein targets TAB2 at Q113-S114, TAK1 at Q360-S361, TAB1 both at Q414-G415 and Q451-S452, and TAB3 at Q173-G174 and Q343-G344. Importantly, overexpression of TAB2 inhibits EV71 replication, whereas addition of cleaved fragments has no effect. Thus, an equilibrium between the TAB2 complex and EV71 3C represents a control point of viral infection. These results suggest that TAK1/TAB1/TAB2/TAB3 cleavage mediated by EV71 may be a mechanism to interfere with inflammatory responses. IMPORTANCE: The TAK1 complex plays a critical role in the activation of NF-κB and cytokine production. However, little is known about its connection to enterovirus 71 (EV71). We demonstrate that EV71 3C suppresses cytokine expression via cleavage of the TAK1 complex proteins. EV71 3C interacts with TAB2 and TAK1. Furthermore, overexpression of TAB2 inhibits EV71 replication, whereas addition of cleaved fragment has no effect. These results suggest that the interplay of EV71 and the TAK1 complex influences the outcome of viral infection.
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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.