ArticleThe Journal of biological chemistry2012
TRIM56 is an essential component of the TLR3 antiviral signaling pathway.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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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, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.
- To TRIM the Immunity: From Innate to Adaptive Immunity.Frontiers in immunology · 2020Pooled it
- TRIM56 Promotes Antiviral Responses Downstream of TLR4.Viruses · 2026Article
- ATG7 Limits Basal Antiviral Gene Expression and Moderately Promotes VSV Replication in Mammalian Non-Immune Cells.Pathogens (Basel, Switzerland) · 2026Article
- Roles and Mechanisms of TRIM Family Proteins in Inflammation in the Brain and Beyond.International journal of molecular sciences · 2026Review
- TRIM proteins as emerging regulators of immune pathways: potential therapeutic targets in immune-related disorders.Frontiers in immunology · 2026Review
- Novel TRIM Proteins Modulating the Innate Immune Response of Rainbow Trout (Animals : an open access journal from MDPI · 2025Article
- The Intrinsic Innate Immunity of Hepatocytes Suppresses HBV Replication and Is Antagonized by HBx.Viruses · 2025Article
- Cytokine-independent induction of LGP2/DHX58 in viral infection.The Journal of general virology · 2025Article
- DNA-RNA hybrids in inflammation: sources, immune response, and therapeutic implications.Journal of molecular medicine (Berlin, Germany) · 2025Review
- TRIM proteins: A 'swiss army knife' of antiviral immunity.PLoS pathogens · 2025Review
- The regulation of innate antiviral immunity by TRIM56.Infectious diseases & immunity · 2025Review
- Epidemiology, Clinical Significance, and Diagnosis of Respiratory Viruses and Their Co-Infections in the Post-COVID Era.Pathogens (Basel, Switzerland) · 2025Review
- Pulmonary embolism in children with mycoplasma pneumonia: can it be predicted?European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025Article
- Emerging Roles of TRIM56 in Antiviral Innate Immunity.Viruses · 2025Review
- Genetic Conservation and Diversity of SARS-CoV-2 Envelope Gene Across Variants of Concern.Journal of medical virology · 2025Article
- Chronic active and chronic inactive hepatitis B virus infection: Comparative study of genetic polymorphism and blood profile measures.PloS one · 2025Article
- Review
- Mechanisms and Assessment of Genotoxicity of Metallic Engineered Nanomaterials in the Human Environment.Biomedicines · 2024Review
- Pulmonary microbial spectrum in late-stage SARS-CoV-2 infection: a case series.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2024Article
- The RNA-binding proteins regulate innate antiviral immune signaling by modulating pattern recognition receptors.Virology journal · 2024Review
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 1 institution in 1 country.
Funding
Abstract
Members of the tripartite motif (TRIM) proteins are being recognized as important regulators of host innate immunity. However, specific TRIMs that contribute to TLR3-mediated antiviral defense have not been identified. We show here that TRIM56 is a positive regulator of TLR3 signaling. Overexpression of TRIM56 substantially potentiated extracellular dsRNA-induced expression of interferon (IFN)-β and interferon-stimulated genes (ISGs), while knockdown of TRIM56 greatly impaired activation of IRF3, induction of IFN-β and ISGs, and establishment of an antiviral state by TLR3 ligand and severely compromised TLR3-mediated chemokine induction following infection by hepatitis C virus. The ability to promote TLR3 signaling was independent of the E3 ubiquitin ligase activity of TRIM56. Rather, it correlated with a physical interaction between TRIM56 and TRIF. Deletion of the C-terminal portion of TRIM56 abrogated the TRIM56-TRIF interaction as well as the augmentation of TLR3-mediated IFN response. Together, our data demonstrate TRIM56 is an essential component of the TLR3 antiviral signaling pathway and reveal a novel role for TRIM56 in innate antiviral immunity.
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What OpenQuestion holds
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.