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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\u2010\u03b2 (IFN\u2010\u03b2), and the IFN\u2010stimulated gene 15 (ISG15) and ISG20 in PRV\u2010infected porcine kidney\u201015 (PK\u201015) cells at 24\u2009h postinfection. Further experiments revealed that RACK1 exerted an inhibitory effect on PRV replication and enhanced the activation of the Type I IFN (IFN\u2010I) signaling pathway. Interestingly, RACK1 was found to facilitate stimulator of IFN genes (STING)\u2013dependent 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\u2010I activation and inhibit PRV infection. These results will provide new data on host factors that limit PRV infection, and facilitate our understanding of IFN\u2010I\u2010mediated antiviral responses during PRV infection.<\/jats:p>","DOI":"10.1155\/tbed\/9584967","type":"journal-article","created":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T08:22:32Z","timestamp":1765441352000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["RACK1 Associates With STING to Promote Type I Interferon Activation and Inhibit Pseudorabies Virus 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