{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T18:18:43Z","timestamp":1791397123340,"version":"4.3.3"},"reference-count":28,"publisher":"American Society for Microbiology","issue":"14","license":[{"start":{"date-parts":[[2013,7,15]],"date-time":"2013-07-15T00:00:00Z","timestamp":1373846400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2013,7,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>Immune evasion by rabies virus depends on targeting of the signal transducers and activator of transcription 1 (STAT1) and STAT2 proteins by the viral interferon antagonist P protein, but targeting of other STAT proteins has not been investigated. Here, we find that P protein associates with activated STAT3 and inhibits STAT3 nuclear accumulation and Gp130-dependent signaling. This is the first report of STAT3 targeting by the interferon antagonist of a virus other than a paramyxovirus, indicating that STAT3 antagonism is important to a range of human-pathogenic viruses.<\/jats:p>","DOI":"10.1128\/jvi.00989-13","type":"journal-article","created":{"date-parts":[[2013,5,23]],"date-time":"2013-05-23T03:51:28Z","timestamp":1369281088000},"page":"8261-8265","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":79,"title":["The Rabies Virus Interferon Antagonist P Protein Interacts with Activated STAT3 and Inhibits Gp130 Receptor Signaling"],"prefix":"10.1128","volume":"87","author":[{"given":"Kim G.","family":"Lieu","sequence":"first","affiliation":[{"name":"Viral Pathogenesis Laboratory, Monash University, Victoria, Australia"},{"name":"Nuclear Signalling Laboratory, Department of Biochemistry and Molecular Biology, Monash University, Victoria, 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