{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T18:25:05Z","timestamp":1791397505734,"version":"4.3.3"},"reference-count":53,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2006,3,15]],"date-time":"2006-03-15T00:00:00Z","timestamp":1142380800000},"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":[[2006,3,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Rabies virus (RV) phosphoprotein P is an interferon (IFN) antagonist counteracting transcriptional activation of type I IFN (K. Brzo\u0301zka, S. Finke, and K. K. Conzelmann, J. Virol\n                    <jats:bold>79:<\/jats:bold>\n                    7673-7681, 2005). We here show that RV P in addition is responsible for preventing IFN-\u03b1\/\u03b2- and IFN-\u03b3-stimulated JAK-STAT signaling in RV-infected cells by the retention of activated STATs in the cytoplasm. Expression of IFN-stimulated response element- and gamma-activated sequence-controlled genes was severely impaired in cells infected with RV SAD L16 or in cells expressing RV P protein from transfected plasmids. In contrast, a recombinant RV expressing small amounts of P had lost the ability to interfere with JAK-STAT signaling. IFN-mediated tyrosine phosphorylation of STAT1 and STAT2 was not impaired in RV P-expressing cells; rather, a defect in STAT recycling was suggested by distinct accumulation of tyrosine-phosphorylated STATs in cell extracts. In the presence of P, activated STAT1 and STAT2 were unable to accumulate in the nucleus. Notably, STAT1 and STAT2 were coprecipitated with RV P only from extracts of cells previously stimulated with IFN-\u03b1 or IFN-\u03b3, whereas in nonstimulated cells no association of P with STATs was observed. This conditional, IFN activation-dependent binding of tyrosine-phosphorylated STATs by RV P is unique for a viral IFN antagonist. The 10 C-terminal residues of P are required for counteracting JAK-STAT signaling but not for inhibition of transcriptional activation of IFN-\u03b2, thus demonstrating two independent functions of RV P in counteracting the host's IFN response.\n                  <\/jats:p>","DOI":"10.1128\/jvi.80.6.2675-2683.2006","type":"journal-article","created":{"date-parts":[[2006,2,24]],"date-time":"2006-02-24T15:47:54Z","timestamp":1140796074000},"page":"2675-2683","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":217,"title":["Inhibition of Interferon Signaling by Rabies Virus Phosphoprotein P: Activation-Dependent Binding of STAT1 and STAT2"],"prefix":"10.1128","volume":"80","author":[{"given":"Krzysztof","family":"Brzo\u0301zka","sequence":"first","affiliation":[{"name":"Max von Pettenkofer Institute and Gene Center, Ludwig-Maximilians-University, D-81377 Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Finke","sequence":"additional","affiliation":[{"name":"Max von Pettenkofer Institute and Gene Center, Ludwig-Maximilians-University, D-81377 Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl-Klaus","family":"Conzelmann","sequence":"additional","affiliation":[{"name":"Max von Pettenkofer Institute and Gene Center, Ludwig-Maximilians-University, D-81377 Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1071545"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri1391"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0407639101"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.molimm.2004.11.007"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.12.7673-7681.2005"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.78.15.8026-8035.2004"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.73.1.251-259.1999"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.9.5374-5385.2005"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.72.3.1925-1930.1998"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.9.5241-5248.2005"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/0042-6822(90)90433-R"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.171.1.267"},{"key":"e_1_3_2_14_2","first-page":"249","volume":"283","year":"2004","unstructured":"Garcia-Sastre, A. 2004. 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