ArticleJournal of virology2012
Foot-and-mouth disease virus 3C protease cleaves NEMO to impair innate immune signaling.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 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.
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Who cites it
113 citing papers in PubMed, 158 citations in OpenAlex.
- Foot-and-mouth disease virus 3C protease as virulence determinant plays multiple roles in cleaving viral polyprotein and host factors.Virulence · 2026Review
- 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
- Viral interference of nucleocytoplasmic transport.The Journal of biological chemistry · 2025Review
- Single-cell RNA sequencing reveals T and B cell-related immune features in foot and mouth disease virus-infected mice.Virulence · 2025Article
- Ubiquitously expressed transcript isoform 2 (UXT-V2) restricts HSV-2 replication by targeting glycoprotein B for degradation through ubiquitin-proteasome pathway.Virologica Sinica · 2025Article
- SADS-CoV nsp5 Inhibits Interferon Production by Targeting Kinase IKKε.Microorganisms · 2025Article
- The pathogenesis of foot-and-mouth disease virus: current understandings and knowledge gaps.Veterinary research · 2025Review
- Foot-and-mouth disease: genomic and proteomic structure, antigenic sites, serotype relationships, immune evasion, recent vaccine development strategies, and future perspectives.Veterinary research · 2025Review
- Limited impact of hepatitis A virus 3C protease-mediated cleavage on the functions of NEMO in human hepatocytes.Journal of virology · 2025Article
- HCoV-229E Mpro Suppresses RLR-Mediated Innate Immune Signalling Through Cleavage of NEMO and Through Other Mechanisms.International journal of molecular sciences · 2025Article
- Review
- Foot-and-mouth disease in Asia.Virus research · 2025Review
- Emerging RNA-centric technologies to probe RNA-protein interactions: importance in decoding the life cycle of positive sense single strand RNA viruses and antiviral discovery.Frontiers in cellular and infection microbiology · 2025Review
- Production of virus-like particles of FMDV by 3C protease cleaving precursor polyprotein P1 in vitro.Applied microbiology and biotechnology · 2024Article
- Review
- Foot-and-mouth disease virus (FMDV) negatively regulates ZFP36 protein expression to alleviate its antiviral activity.Journal of virology · 2024Article
- Article
- Article
- Classical swine fever virus NS5A protein antagonizes innate immune response by inhibiting the NF-κB signaling.Virologica Sinica · 2023Article
- 3CVirologica Sinica · 2023Article
53 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
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Foot-and-mouth disease is a highly contagious viral illness of wild and domestic cloven-hoofed animals. The causative agent, foot-and-mouth disease virus (FMDV), replicates rapidly, efficiently disseminating within the infected host and being passed on to susceptible animals via direct contact or the aerosol route. To survive in the host, FMDV has evolved to block the host interferon (IFN) response. Previously, we and others demonstrated that the leader proteinase (L(pro)) of FMDV is an IFN antagonist. Here, we report that another FMDV-encoded proteinase, 3C(pro), also inhibits IFN-α/β response and the expression of IFN-stimulated genes. Acting in a proteasome- and caspase-independent manner, the 3C(pro) of FMDV proteolytically cleaved nuclear transcription factor kappa B (NF-κB) essential modulator (NEMO), a bridging adaptor protein essential for activating both NF-κB and interferon-regulatory factor signaling pathways. 3C(pro) specifically targeted NEMO at the Gln 383 residue, cleaving off the C-terminal zinc finger domain from the protein. This cleavage impaired the ability of NEMO to activate downstream IFN production and to act as a signaling adaptor of the RIG-I/MDA5 pathway. Mutations specifically disrupting the cysteine protease activity of 3C(pro) abrogated NEMO cleavage and the inhibition of IFN induction. Collectively, our data identify NEMO as a substrate for FMDV 3C(pro) and reveal a novel mechanism evolved by a picornavirus to counteract innate immune signaling.
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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.