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Article: Perturbation of biogenesis and targeting of Epstein-Barr virus-encoded miR-BART3 microRNA by adenosine-to-inosine editing

TitlePerturbation of biogenesis and targeting of Epstein-Barr virus-encoded miR-BART3 microRNA by adenosine-to-inosine editing
Authors
Issue Date2013
PublisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.org
Citation
Journal of General Virology, 2013, v. 94 n. pt. 12, p. 2739-2744 How to Cite?
AbstractEpstein-Barr virus (EBV) encodes at least 44 mature microRNAs (miRNAs), some of which are abundantly expressed in nasopharyngeal carcinoma cells. EBV-encoded miR-BART6 miRNA is known to undergo adenosine-to-inosine (A-to-I) RNA editing, which impacts on processing and function. Whether additional EBV miRNAs might be A-to-I edited remains to be determined. In this study, we have reported on A-to-I editing of EBV miR-BART3. The A-to-I editing enzyme was expressed abundantly in EBV-infected epithelial carcinoma cells. pri-miR-BART3 was found to be edited at four sites in these cells and in nasopharyngeal carcinoma samples. Whereas editing of the second site located within the seed region prevented the targeting of DICE1 mRNA, editing of the third site effectively crippled the biogenesis of mature miR-BART3. Thus, A-to-I editing perturbs biogenesis and targeting of miR-BART3 and may contribute to its differential expression and function in EBV-infected epithelial cells. © 2013 SGM.
Persistent Identifierhttp://hdl.handle.net/10722/200453
ISSN
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 0.990
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLei, T-
dc.contributor.authorYuen, KS-
dc.contributor.authorTsao, GSW-
dc.contributor.authorChen, H-
dc.contributor.authorKok, KH-
dc.contributor.authorJin, D-
dc.date.accessioned2014-08-21T06:46:36Z-
dc.date.available2014-08-21T06:46:36Z-
dc.date.issued2013-
dc.identifier.citationJournal of General Virology, 2013, v. 94 n. pt. 12, p. 2739-2744-
dc.identifier.issn0022-1317-
dc.identifier.urihttp://hdl.handle.net/10722/200453-
dc.description.abstractEpstein-Barr virus (EBV) encodes at least 44 mature microRNAs (miRNAs), some of which are abundantly expressed in nasopharyngeal carcinoma cells. EBV-encoded miR-BART6 miRNA is known to undergo adenosine-to-inosine (A-to-I) RNA editing, which impacts on processing and function. Whether additional EBV miRNAs might be A-to-I edited remains to be determined. In this study, we have reported on A-to-I editing of EBV miR-BART3. The A-to-I editing enzyme was expressed abundantly in EBV-infected epithelial carcinoma cells. pri-miR-BART3 was found to be edited at four sites in these cells and in nasopharyngeal carcinoma samples. Whereas editing of the second site located within the seed region prevented the targeting of DICE1 mRNA, editing of the third site effectively crippled the biogenesis of mature miR-BART3. Thus, A-to-I editing perturbs biogenesis and targeting of miR-BART3 and may contribute to its differential expression and function in EBV-infected epithelial cells. © 2013 SGM.-
dc.languageeng-
dc.publisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.org-
dc.relation.ispartofJournal of General Virology-
dc.rightsJournal of General Virology. Copyright © Society for General Microbiology.-
dc.titlePerturbation of biogenesis and targeting of Epstein-Barr virus-encoded miR-BART3 microRNA by adenosine-to-inosine editing-
dc.typeArticle-
dc.identifier.emailTsao, GSW: gswtsao@hku.hk-
dc.identifier.emailChen, H: hlchen@hku.hk-
dc.identifier.emailKok, KH: khkok@hku.hk-
dc.identifier.emailJin, D: dyjin@hku.hk-
dc.identifier.authorityTsao, GSW=rp00399-
dc.identifier.authorityChen, H=rp00383-
dc.identifier.authorityKok, KH=rp01455-
dc.identifier.authorityJin, D=rp00452-
dc.identifier.doi10.1099/vir.0.056226-0-
dc.identifier.pmid24045110-
dc.identifier.scopuseid_2-s2.0-84887536769-
dc.identifier.hkuros234932-
dc.identifier.volume94-
dc.identifier.issuept. 12-
dc.identifier.spage2739-
dc.identifier.epage2744-
dc.identifier.isiWOS:000328808000018-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl0022-1317-

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