{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T18:18:12Z","timestamp":1791397092253,"version":"4.3.3"},"reference-count":28,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2007,4,15]],"date-time":"2007-04-15T00:00:00Z","timestamp":1176595200000},"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":[[2007,4,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>Rabies virus P protein inhibits alpha interferon (IFN-\u03b1)- and IFN-\u03b3-stimulated Jak-STAT signaling by retaining phosphorylated STAT1 in the cytoplasm. Here, we show that P also blocks an intranuclear step that is the STAT1 binding to the DNA promoter of IFN-responsive genes. As P is a nucleocytoplasmic shuttling protein, we first investigated the effect of the cellular distribution of P on the localization of STAT1 and consequently on IFN signaling. We show that the localization of STAT1 is correlated with the localization of P: in cells expressing a nuclear form of P (the short P3 isoform or the complete P in the presence of the export inhibitor leptomycin B), STAT1 is nuclear, whereas in cells expressing a cytoplasmic form of P, STAT1 is cytoplasmic. However, the expression of nuclear forms of P inhibits the signaling of both IFN-\u03b3 and IFN-\u03b1, demonstrating that the retention of STAT1 in the cytoplasm is not the only mechanism involved in the inhibition of IFN signaling. Electrophoretic mobility shift analysis indicates that P expression in the cell extracts of infected cells or in stable cell lines prevents IFN-induced DNA binding of STAT1. The loss of the DNA binding of STAT1 and ISGF3 was also observed when purified recombinant P or P3 was added to the extracts of IFN-\u03b3- or IFN-\u03b1-treated cells, indicating that P directly affects the DNA binding activity of STAT1. Then products of the rabies virus P gene are able to counteract IFN signaling by creating both cytoplasmic and nuclear blocks for STAT1.<\/jats:p>","DOI":"10.1128\/jvi.01930-06","type":"journal-article","created":{"date-parts":[[2007,2,8]],"date-time":"2007-02-08T01:19:35Z","timestamp":1170897575000},"page":"4255-4263","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":157,"title":["The Nucleocytoplasmic Rabies Virus P Protein Counteracts Interferon Signaling by Inhibiting both Nuclear Accumulation and DNA Binding of STAT1"],"prefix":"10.1128","volume":"81","author":[{"given":"Aurore","family":"Vidy","sequence":"first","affiliation":[{"name":"FRE 2944 CNRS, Institut Lwoff, 7 rue Guy Moquet, 94801 Villejuif, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jamila","family":"El Bougrini","sequence":"additional","affiliation":[{"name":"FRE 2944 CNRS, Institut Lwoff, 7 rue Guy Moquet, 94801 Villejuif, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mounira K.","family":"Chelbi-Alix","sequence":"additional","affiliation":[{"name":"FRE 2944 CNRS, Institut Lwoff, 7 rue Guy Moquet, 94801 Villejuif, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Danielle","family":"Blondel","sequence":"additional","affiliation":[{"name":"CNRS, UMR2472, IFR 115, and INRA, UMR1157, Virologie Mole\u0301culaire et Structurale, 91198 Gif sur Yvette, France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1080\/08830180213277"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.190318397"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1205931"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.12.7673-7681.2005"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.80.6.2675-2683.2006"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1089\/jir.2006.26.271"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.69.2.707-712.1995"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.8197455"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1286-4579(02)01583-6"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.74.19.8823-8830.2000"},{"key":"e_1_3_2_12_2","first-page":"1757","volume":"81","year":"2000","unstructured":"Gigant, B., F. Iseni, Y. Gaudin, M. Knossow, and D. Blondel. 2000. Neither phosphorylation nor the amino-terminal part of rabies virus phosphoprotein is required for its oligomerization. J. Gen. Virol.81:1757-1761.","journal-title":"J. Gen. Virol."},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1099\/0022-1317-81-10-2341"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0042-6822(03)00590-7"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.74.1.91-98.2000"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.virol.2005.09.024"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cytogfr.2004.02.003"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/21.3.344"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1101\/gad.268003"},{"key":"e_1_3_2_20_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M400766200"},{"key":"e_1_3_2_21_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.virol.2005.02.005"},{"key":"e_1_3_2_22_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1201410"},{"key":"e_1_3_2_23_2","doi-asserted-by":"publisher","DOI":"10.1099\/0022-1317-78-1-119"},{"key":"e_1_3_2_24_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.74.21.10212-10216.2000"},{"key":"e_1_3_2_25_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1204854"},{"key":"e_1_3_2_26_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.78.10.5358-5367.2004"},{"key":"e_1_3_2_27_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.78.11.5633-5641.2004"},{"key":"e_1_3_2_28_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.10.6078-6088.2005"},{"key":"e_1_3_2_29_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.22.14411-14420.2005"}],"container-title":["Journal of Virology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.asm.org\/doi\/pdf\/10.1128\/JVI.01930-06","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.asm.org\/doi\/pdf\/10.1128\/JVI.01930-06","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,5]],"date-time":"2022-03-05T11:45:08Z","timestamp":1646480708000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.asm.org\/doi\/10.1128\/JVI.01930-06"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2007,4,15]]},"references-count":28,"journal-issue":{"issue":"8","published-print":{"date-parts":[[2007,4,15]]}},"alternative-id":["10.1128\/JVI.01930-06"],"URL":"https:\/\/doi.org\/10.1128\/jvi.01930-06","relation":{},"ISSN":["0022-538X","1098-5514"],"issn-type":[{"value":"0022-538X","type":"print"},{"value":"1098-5514","type":"electronic"}],"subject":[],"published":{"date-parts":[[2007,4,15]]},"assertion":[{"value":"2006-09-05","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2007-01-29","order":1,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2007-04-15","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}