ArticleTransboundary and emerging diseases2025
RACK1 Associates With STING to Promote Type I Interferon Activation and Inhibit Pseudorabies Virus Infection.
Article in Transboundary and emerging diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- RACK1 inhibits fowl adenovirus serotype 4 replication by targeting the viral protein Hexon for ubiquitin-proteasome degradation.Poultry science · 2026Article
- 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
- RACK1 in host immune response to infections: molecular mechanisms and therapeutic potentials.Frontiers in immunology · 2026Review
- Organelle-centered ISG15 biology: distinguishing covalent ISGylation from interferon-associated responses.Frontiers in immunology · 2026Review
- RACK1 Associates With STING to Promote Type I Interferon Activation and Inhibit Pseudorabies Virus Infection.Transboundary and emerging diseases · 2025Article
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Authors and funding
9 authors.
Funding
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Abstract
Pseudorabies virus (PRV), the causative agent of Aujeszky's disease, leads to great economic losses on swine production worldwide. Receptor of activated protein kinase C 1 (RACK1) is initially known as a receptor for protein kinase C, and recent studies indicate that RACK1 can also play critical roles in various virus infections. However, the role of RACK1 during PRV infection has not yet been determined. In this investigation, we observed a strong positive correlation between the expression levels of RACK1, interferon-β (IFN-β), and the IFN-stimulated gene 15 (ISG15) and ISG20 in PRV-infected porcine kidney-15 (PK-15) cells at 24 h postinfection. Further experiments revealed that RACK1 exerted an inhibitory effect on PRV replication and enhanced the activation of the Type I IFN (IFN-I) signaling pathway. Interestingly, RACK1 was found to facilitate stimulator of IFN genes (STING)-dependent phosphorylation of IFN regulatory factor 3 (IRF3). More specifically, RACK1 could interact with STING and then promote aggregation of STING around the Golgi apparatus. Taken together, these findings demonstrated that RACK1 could associate with STING to promote IFN-I activation and inhibit PRV infection. These results will provide new data on host factors that limit PRV infection, and facilitate our understanding of IFN-I-mediated antiviral responses during PRV infection.
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