ArticleFrontiers in immunology2020
Duck TRIM32 Functions in IFN-β Signaling Against the Infection of H5N6 Highly Pathogenic Avian Influenza Virus.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Seneca Valley virus 3C protease targets TRIM32 for cleavage to antagonize its antiviral effects.Journal of virology · 2025Article
- Antiviral Effects of Avian Interferon-Stimulated Genes.Animals : an open access journal from MDPI · 2024Review
- Proteomics Analysis of Duck Lung Tissues in Response to Highly Pathogenic Avian Influenza Virus.Microorganisms · 2024Article
- 4E-BP1-dependent translation in nociceptors controls mechanical hypersensitivity via TRIM32/type I interferon signaling.Science advances · 2023Article
- The ubiquitin ligase TRIM32 promotes the autophagic response to Mycobacterium tuberculosis infection in macrophages.Cell death & disease · 2023Article
- Evolution and expression of the duck TRIM gene repertoire.Frontiers in immunology · 2023Article
- Article
- Duck TRIM29 negatively regulates type I IFN production by targeting MAVS.Frontiers in immunology · 2022Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammals, tripartite motif 32 (TRIM32) is essential for regulating host innate immune responses to viral infections. However, the antiviral effect of TRIM32 in birds has not been reported. Here, we cloned the full-length duck TRIM32 (duTRIM32) cDNA from total spleen RNA of Peking duck. DuTRIM32 consists of 682 amino acids and has 95.5% similarity in amino acid sequences with chicken TRIM32 and 84.9% similarity with human TRIM32, respectively. DuTRIM32 mRNA was found to be ubiquitously expressed in all tested tissues from healthy ducks. Overexpression of duTRIM32 significantly activated the IFN-β promoter and upregulated the mRNA levels of IFN-β, IRF7, and Mx, which indicates that duTRIM32 is involved in the type I IFN pathway. Furthermore, duTRIM32 was found to directly interact with duck STING (duSTING) and to contribute to the expression of IFN-β mediated by duSTING. The mRNA level of duTRIM32 was significantly upregulated in the lungs and spleens of H5N6 highly pathogenic avian influenza virus (HPAIV) infected ducks 3 days post-infection (DPI). Furthermore, overexpression of duTRIM32 could inhibit the replication of H5N6 HPAIV in duck embryo fibroblasts (DEFs). Therefore, these results indicate that duTRIM32 is involved in the type I IFN pathway and exhibit an antiviral effect against H5N6 HPAIV infection.
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