Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/348415
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampSecolin, Rodrigo-
dc.contributor.authorunicampLopes-Cendes, Íscia Teresinha-
dc.typeArtigopt_BR
dc.titleAnalysis of energetically biased transcripts of viruses and transposable elementspt_BR
dc.contributor.authorSecolin, Rodrigo-
dc.contributor.authorBitencourt Pascoal, Vinicius D'Avila-
dc.contributor.authorLopes-Cendes, Iscia-
dc.contributor.authorPereira, Tiago Campos-
dc.subjectRNA interferente pequenopt_BR
dc.subject.otherlanguageRNA, Small Interferingpt_BR
dc.description.abstractRNA interference (RNAi) is a natural endogenous process by which double-stranded RNA molecules trigger potent and specific gene silencing in eukaryotic cells and is characterized by target RNA cleavage. In mammals, small interfering RNAs (siRNAs) are the trigger molecules of choice and constitute a new class of RNA-based antiviral agents. In an efficient RNAi response, the antisense strand of siRNAs must enter the RNA-induced silencing complex (RISC) in a process mediated by thermodynamic features. In this report, we hypothesize that silent mutations capable of inverting thermodynamic properties can promote resistance to siRNAs. Extensive computational analyses were used to assess whether continuous selective pressure that promotes such mutations could lead to the emergence of viral strains completely resistant to RNAi (i.e., prone to transfer only the sense strands to RISC). Based on our findings, we propose that, although synonymous mutations may produce functional resistance, this strategy cannot be systematically adopted by viruses since the longest RNAi-refractory sequence is only 10 nt long. This finding also suggests that all mRNAs display fluctuating thermodynamic landscapes and that, in terms of thermodynamic features, RNAi is a very efficient antiviral system since there will always be sites susceptible to siRNAspt_BR
dc.relation.ispartofGenetics and molecular biologypt_BR
dc.relation.ispartofabbreviationGenet mol. biolpt_BR
dc.publisher.cityRibeirão Preto, SPpt_BR
dc.publisher.countryBrasilpt_BR
dc.publisherSociedade Brasileira de Genéticapt_BR
dc.date.issued2012-
dc.date.monthofcirculationDec.pt_BR
dc.language.isoengpt_BR
dc.description.volume35pt_BR
dc.description.issuenumber4pt_BR
dc.description.firstpage868pt_BR
dc.description.lastpage873pt_BR
dc.rightsAbertopt_BR
dc.sourceSciELOpt_BR
dc.identifier.issn1415-4757pt_BR
dc.identifier.eissn1678-4685pt_BR
dc.identifier.doi10.1590/S1415-47572012005000078pt_BR
dc.identifier.urlhttps://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572012000500022pt_BR
dc.description.sponsorshipCONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQpt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.date.available2020-09-01T12:24:20Z-
dc.date.accessioned2020-09-01T12:24:20Z-
dc.description.provenanceSubmitted by Cintia Oliveira de Moura (cintiaom@unicamp.br) on 2020-09-01T12:24:20Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-01-04T15:14:47Z : No. of bitstreams: 1 S1415-47572012000500022.pdf: 1841754 bytes, checksum: 230f9be202f67ed525ecb435f21f6b5f (MD5)en
dc.description.provenanceMade available in DSpace on 2020-09-01T12:24:20Z (GMT). No. of bitstreams: 0 Previous issue date: 2012en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/348415-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Genética Médicapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.subject.keywordSynonymous mutationpt_BR
dc.subject.keywordViral evolutionpt_BR
dc.identifier.sourceS1415-47572012000500022pt_BR
dc.creator.orcid0000-0002-2485-9560pt_BR
dc.creator.orcid0000-0002-6221-6822pt_BR
dc.type.formArtigopt_BR
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