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Article: Utility of Epstein-Barr virus-encoded small RNA promoters for driving the expression of fusion transcripts harboring short hairpin RNAs

TitleUtility of Epstein-Barr virus-encoded small RNA promoters for driving the expression of fusion transcripts harboring short hairpin RNAs
Authors
KeywordsSpecies Index: Human Herpesvirus 4
Mammalia
Issue Date2008
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/gt
Citation
Gene Therapy, 2008, v. 15 n. 3, p. 191-202 How to Cite?
AbstractTo induce RNA interference (RNAi), either small interfering RNAs (siRNAs) are directly introduced into the cell or short hairpin RNAs (shRNAs) are expressed from a DNA vector. At present, shRNAs are commonly synthesized by RNA polymerase III (Pol III) promoters of the H1 and U6 RNAs. In this study, we designed and characterized a new set of plasmid vectors driven by promoters of the Epstein-Barr virus (EBV)-encoded small RNAs (EBERs). The EBERs are the most abundant transcript in infected cells and they are transcribed by Pol III. We showed that the EBER promoters were able to drive the expression of shRNA fusion transcripts. siRNAs processed from these fusion transcripts specifically and effectively inhibited the expression of homologous reporter or endogenous genes in various types of cells. The partial EBER sequences in the fusion transcripts did not activate double-stranded RNA-dependent protein kinase or suppress RNAi. In nasopharyngeal carcinoma cells, the EBER2 promoter was stronger than the H1 and U6 promoters in shRNA synthesis, leading to more effective knockdown of the target genes. Taken together, our findings suggest that the EBER promoters fundamentally different from those of H1 and U6 can be used to drive the intracellular expression of shRNAs for effective silencing of target genes in mammalian cells and particularly, in EBV-infected cells.
Persistent Identifierhttp://hdl.handle.net/10722/132359
ISSN
2015 Impact Factor: 3.242
2015 SCImago Journal Rankings: 1.519
ISI Accession Number ID
References
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DC FieldValueLanguage
dc.contributor.authorChoy, EYWen_HK
dc.contributor.authorKok, KHen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorJin, DYen_HK
dc.date.accessioned2011-03-28T09:23:34Z-
dc.date.available2011-03-28T09:23:34Z-
dc.date.issued2008en_HK
dc.identifier.citationGene Therapy, 2008, v. 15 n. 3, p. 191-202en_HK
dc.identifier.issn0969-7128en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132359-
dc.description.abstractTo induce RNA interference (RNAi), either small interfering RNAs (siRNAs) are directly introduced into the cell or short hairpin RNAs (shRNAs) are expressed from a DNA vector. At present, shRNAs are commonly synthesized by RNA polymerase III (Pol III) promoters of the H1 and U6 RNAs. In this study, we designed and characterized a new set of plasmid vectors driven by promoters of the Epstein-Barr virus (EBV)-encoded small RNAs (EBERs). The EBERs are the most abundant transcript in infected cells and they are transcribed by Pol III. We showed that the EBER promoters were able to drive the expression of shRNA fusion transcripts. siRNAs processed from these fusion transcripts specifically and effectively inhibited the expression of homologous reporter or endogenous genes in various types of cells. The partial EBER sequences in the fusion transcripts did not activate double-stranded RNA-dependent protein kinase or suppress RNAi. In nasopharyngeal carcinoma cells, the EBER2 promoter was stronger than the H1 and U6 promoters in shRNA synthesis, leading to more effective knockdown of the target genes. Taken together, our findings suggest that the EBER promoters fundamentally different from those of H1 and U6 can be used to drive the intracellular expression of shRNAs for effective silencing of target genes in mammalian cells and particularly, in EBV-infected cells.en_HK
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/gten_HK
dc.relation.ispartofGene Therapyen_HK
dc.subjectSpecies Index: Human Herpesvirus 4en_US
dc.subjectMammaliaen_US
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshFeasibility Studiesen_HK
dc.subject.meshGene Expressionen_HK
dc.subject.meshGene Silencingen_HK
dc.subject.meshGene Therapy - methodsen_HK
dc.subject.meshGenetic Engineeringen_HK
dc.subject.meshGenetic Vectors - pharmacologyen_HK
dc.subject.meshHerpesvirus 4, Human - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshNasopharyngeal Neoplasms - metabolism - therapyen_HK
dc.subject.meshPromoter Regions, Geneticen_HK
dc.subject.meshRNA Interferenceen_HK
dc.subject.meshRNA Polymerase III - geneticsen_HK
dc.subject.meshRNA, Messenger - analysisen_HK
dc.subject.meshRNA, Small Interferingen_HK
dc.subject.meshRecombinant Fusion Proteins - geneticsen_HK
dc.titleUtility of Epstein-Barr virus-encoded small RNA promoters for driving the expression of fusion transcripts harboring short hairpin RNAsen_HK
dc.typeArticleen_HK
dc.identifier.emailKok, KH:khkok@hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.authorityKok, KH=rp01455en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.gt.3303055en_HK
dc.identifier.pmid17972920-
dc.identifier.scopuseid_2-s2.0-38549179369en_HK
dc.identifier.hkuros151302-
dc.identifier.hkuros139250-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-38549179369&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume15en_HK
dc.identifier.issue3en_HK
dc.identifier.spage191en_HK
dc.identifier.epage202en_HK
dc.identifier.eissn1476-5462-
dc.identifier.isiWOS:000252585100005-
dc.publisher.placeUnited Kingdomen_HK
dc.relation.projectDevelopment of novel nucleic acid therapeutics for viral infection and cancer-
dc.relation.projectMitotic checkpoint and genomic stability in ovarian cancer-
dc.identifier.scopusauthoridChoy, EYW=23476516200en_HK
dc.identifier.scopusauthoridKok, KH=7006862631en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.citeulike1852207-

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