{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T11:24:33Z","timestamp":1791199473514,"version":"4.2.0"},"reference-count":29,"publisher":"National Academy of Sciences","issue":"32","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2009,8,11]]},"abstract":"<jats:p>\n                    Inevitably, viruses depend on host factors for their multiplication. Here, we show that hepatitis C virus (HCV) RNA translation and replication depends on Rck\/p54, LSm1, and PatL1, which regulate the fate of cellular mRNAs from translation to degradation in the 5\u2032-3\u2032-deadenylation-dependent mRNA decay pathway. The requirement of these proteins for efficient HCV RNA translation was linked to the 5\u2032 and 3\u2032 untranslated regions (UTRs) of the viral genome. Furthermore, LSm1\u20137 complexes specifically interacted with essential\n                    <jats:italic>cis<\/jats:italic>\n                    -acting HCV RNA elements located in the UTRs. These results bridge HCV life cycle requirements and highly conserved host proteins of cellular mRNA decay. The previously described role of these proteins in the replication of 2 other positive-strand RNA viruses, the plant brome mosaic virus and the bacteriophage Q\u00df, pinpoint a weak spot that may be exploited to generate broad-spectrum antiviral drugs.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0906413106","type":"journal-article","created":{"date-parts":[[2009,7,23]],"date-time":"2009-07-23T21:36:29Z","timestamp":1248384989000},"page":"13517-13522","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":127,"title":["Translation and replication of hepatitis C virus genomic RNA depends on ancient cellular proteins that control mRNA fates"],"prefix":"10.1073","volume":"106","author":[{"given":"Nicoletta","family":"Scheller","sequence":"first","affiliation":[{"name":"Department of Experimental and Health Sciences, Universitat Pompeu Fabra, 08003 Barcelona, Spain;"},{"name":"Institute of Virology, Saarland University, D-66421 Homburg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leonardo Bruno","family":"Mina","sequence":"additional","affiliation":[{"name":"Department of Experimental and Health Sciences, Universitat Pompeu Fabra, 08003 Barcelona, Spain;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui Pedro","family":"Gal\u00e3o","sequence":"additional","affiliation":[{"name":"Department of Experimental and Health Sciences, Universitat Pompeu Fabra, 08003 Barcelona, Spain;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ashwin","family":"Chari","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Biocenter, University of Wuerzburg, Am Hubland, D-97074 Wuerzburg, Germany; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mireia","family":"Gim\u00e9nez-Barcons","sequence":"additional","affiliation":[{"name":"Department of Experimental and Health Sciences, Universitat Pompeu Fabra, 08003 Barcelona, 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