{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T18:18:33Z","timestamp":1791397113063,"version":"4.3.3"},"reference-count":38,"publisher":"American Society for Microbiology","issue":"20","license":[{"start":{"date-parts":[[2010,10,15]],"date-time":"2010-10-15T00:00:00Z","timestamp":1287100800000},"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":[[2010,10,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Various reports implicate PML and PML nuclear bodies (NBs) in an intrinsic antiviral response targeting diverse cytoplasmic replicating RNA viruses. PML conjugation to the small ubiquitin-like modifier (SUMO) is required for its localization within NBs. PML displays antiviral effects\n            <jats:italic>in vivo<\/jats:italic>\n            , as PML deficiency renders mice more susceptible to infection with the rhabdovirus vesicular stomatitis virus (VSV). Cells derived from these mice are also more sensitive to infection with rabies virus, another member of the rhabdovirus family. Alternative splicing from a single gene results in the synthesis of several PML isoforms, and these are classified into seven groups, designated PMLI to -VII. We report here that expression of PMLIV or PMLIVa, which is missing exon 5, inhibited viral mRNA and protein synthesis, leading to a reduction in viral replication. However, the expression of other nuclear isoforms (PMLI to -VI) and cytoplasmic PMLVIIb failed to impair viral production. This antiviral effect required PMLIV SUMOylation, as it was not observed with PMLIV 3KR, in which the lysines involved in SUMO conjugation were mutated. Thus, PMLIV and PMLIVa may exert this isoform-specific function through interaction with specific NB protein partners via their common C-terminal region.\n          <\/jats:p>","DOI":"10.1128\/jvi.01286-10","type":"journal-article","created":{"date-parts":[[2010,8,12]],"date-time":"2010-08-12T02:28:22Z","timestamp":1281580102000},"page":"10719-10726","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":68,"title":["Resistance to Rabies Virus Infection Conferred by the PMLIV Isoform"],"prefix":"10.1128","volume":"84","author":[{"given":"Danielle","family":"Blondel","sequence":"first","affiliation":[{"name":"UPR 3296 CNRS, 91198 Gif sur Yvette, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabrina","family":"Kheddache","sequence":"additional","affiliation":[{"name":"CNRS, FRE 3235, Universite\u0301 Paris Descartes, 75006 Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xavier","family":"Lahaye","sequence":"additional","affiliation":[{"name":"UPR 3296 CNRS, 91198 Gif sur Yvette, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laurent","family":"Dianoux","sequence":"additional","affiliation":[{"name":"CNRS, FRE 3235, Universite\u0301 Paris Descartes, 75006 Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mounira K.","family":"Chelbi-Alix","sequence":"additional","affiliation":[{"name":"CNRS, FRE 3235, Universite\u0301 Paris Descartes, 75006 Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1147"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1205931"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.76.8.3810-3818.2002"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.72.5.3819-3826.1998"},{"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","first-page":"2027","volume":"9","year":"1995","unstructured":"Chelbi-Alix, M. 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