ArticleInternational journal of molecular sciences2023
TRIM21 Promotes Rabies Virus Production by Degrading IRF7 through Ubiquitination.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Dog bite-associated pathogens: advances in pathogenic mechanisms and systemic clinical consequences in humans.One health (Amsterdam, Netherlands) · 2026Review
- Unraveling the Multifaceted Role of TRIM21 in Virus-Triggered Innate Immunity and Diseases.Biomolecules · 2026Review
- TRIM21 is a molecular rheostat for influenza A virus replication.bioRxiv : the preprint server for biology · 2026Article
- RND3 restricts encephalomyocarditis virus replication by promoting IKKε ubiquitination and type I interferon production.Microbiology spectrum · 2026Article
- OLFML3 negatively regulates RIG-I signaling in RNA virus infection.Frontiers in immunology · 2026Article
- Ferroptosis in veterinary medicine: mechanisms, therapies, and unmet challenges.The veterinary quarterly · 2025Review
- Selective Autophagy Mediated by Protein Ubiquitination in Major Prevalent Zoonoses.Transboundary and emerging diseases · 2025Review
- TRIM44 Promotes Rabies Virus Replication by Autophagy-Dependent Mechanism.International journal of molecular sciences · 2024Article
- 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
- Human Rabies Treatment-From Palliation to Promise.Viruses · 2024Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rabies, a highly fatal zoonotic disease, is a significant global public health threat. Currently, the pathogenic mechanism of rabies has not been fully elucidated, and no effective treatment for rabies is available. Increasing evidence shows that the tripartite-motif protein (TRIM) family of proteins participates in the host's regulation of viral replication. Studies have demonstrated the upregulated expression of tripartite-motif protein 21 (TRIM21) in the brain tissue of mice infected with the rabies virus. Related studies have shown that TRIM21 knockdown inhibits RABV replication, while overexpression of TRIM21 exerted the opposite effect. Knockdown of interferon-alpha and interferon-beta modulates the inhibition of RABV replication caused by TRIM21 knockdown and promotes the replication of the virus. Furthermore, our previous study revealed that TRIM21 regulates the secretion of type I interferon during RABV infection by targeting interferon regulatory factor 7 (IRF7). IRF7 knockdown reduced the inhibition of RABV replication caused by the knockdown of TRIM21 and promoted viral replication. TRIM21 regulates RABV replication via the IRF7-IFN axis. Our study identified TRIM21 as a novel host factor required by RABV for replication. Thus, TRIM21 is a potential target for rabies treatment or management.
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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.