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dc.contributor.authorColaço, Camila Schoueri-
dc.contributor.authorMatos, Adriano Reis de-
dc.contributor.authorEstrêla, Martha Silva-
dc.contributor.authorRocha Júnior, Maurício Cristiano-
dc.contributor.authorOtaguiri, Kátia Kaori-
dc.contributor.authorRodrigues, Evandra Strazza-
dc.contributor.authorTakayanagui, Osvaldo Massaiti-
dc.contributor.authorCovas, Dimas Tadeu-
dc.contributor.authorKashima, Simone-
dc.contributor.authorPittella-Silva, Fabio-
dc.contributor.authorHaddad, Rodrigo-
dc.date.accessioned2022-10-03T14:37:30Z-
dc.date.available2022-10-03T14:37:30Z-
dc.date.issued2017-06-12-
dc.identifier.citationCOLAÇO, Camila Schoueri et al. Downregulation of histone methyltransferase EHMT2 in CD4+ T-cells may protect HTLV-1-infected individuals against HAM/TSP development. Archives of Virology, v. 162, p. 3131-3136, 2017. DOI: https://doi.org/10.1007/s00705-017-3428-8.pt_BR
dc.identifier.urihttps://repositorio.unb.br/handle/10482/44950-
dc.language.isoInglêspt_BR
dc.publisherSpringerpt_BR
dc.rightsAcesso Restritopt_BR
dc.titleDownregulation of histone methyltransferase EHMT2 in CD4+ T-cells may protect HTLV-1-infected individuals against HAM/TSP developmentpt_BR
dc.typeArtigopt_BR
dc.subject.keywordVírus da leucemiapt_BR
dc.subject.keywordMielopatiapt_BR
dc.subject.keywordHistonaspt_BR
dc.subject.keywordMetiltransferasespt_BR
dc.identifier.doihttps://doi.org/10.1007/s00705-017-3428-8pt_BR
dc.relation.publisherversionhttps://link.springer.com/article/10.1007/s00705-017-3428-8pt_BR
dc.description.abstract1Approximately 5% of human T-cell leukemia virus type 1 (HTLV-1)-infected individuals will develop one of the HTLV-1-related diseases, such as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) or adult T-cell leukemia. However, the mechanisms responsible for the appearance of symptoms have not been fully clarified. It is believed that viral factors, host genetic and epigenetic mechanisms are implicated in this process. Studies have shown the involvement of histone methyltransferases in retrovirus infection, but no study observed their expression in HTLV-1-infected patients. Among them, euchromatic histone-lysine N-methyltransferase (EHMT)-1 and EHMT-2 were related to retroviral latency in HIV-1 infection. We investigated whether histone methyltransferases EHMT1 and EHMT2 exert any influence on HAM/TSP development by assessing their expression levels in CD4+ T-cells from HTLV–1–infected patients. CD4+ T-cells were immunomagnetically isolated from peripheral blood mononuclear cells of HTLV-1-infected or non–infected individuals and the expression levels of EHMT1 and EHMT2 were determined by RT-qPCR. We observed that EHMT2 was negatively regulated in HTLV-1 asymptomatic carriers compared to non-infected individuals. No difference was observed for EHMT1. These results suggest that EHMT2 downregulation in CD4+ T-cells may be linked to a protection mechanism against the development of HAM/TSP.pt_BR
dc.contributor.affiliationUniversidade de Brasília, Faculdade de Ciências da Saúde, Laboratório de Patologia Molecular do Câncerpt_BR
dc.contributor.affiliationUniversidade de Brasília, Faculdade de Ciências da Saúde, Laboratório de Patologia Molecular do Câncerpt_BR
dc.contributor.affiliationUniversidade de Brasília, Faculdade de Ciências da Saúde, Laboratório de Patologia Molecular do Câncerpt_BR
dc.contributor.affiliationUniversidade de São Paulo, Centro de Hemoterapia de Ribeirão Pretopt_BR
dc.contributor.affiliationUniversidade de São Paulo, Centro de Hemoterapia de Ribeirão Pretopt_BR
dc.contributor.affiliationUniversidade de São Paulo, Centro de Hemoterapia de Ribeirão Pretopt_BR
dc.contributor.affiliationUniversidade de São Paulo, Centro de Hemoterapia de Ribeirão Pretopt_BR
dc.contributor.affiliationUniversidade de São Paulo, Centro de Hemoterapia de Ribeirão Pretopt_BR
dc.contributor.affiliationUniversidade de São Paulo, Centro de Hemoterapia de Ribeirão Pretopt_BR
dc.contributor.affiliationUniversidade de Brasília, Faculdade de Ciências da Saúde, Laboratório de Patologia Molecular do Câncerpt_BR
dc.contributor.affiliationUniversidade de Brasília, Faculdade de Ciências da Saúde, Laboratório de Patologia Molecular do Câncerpt_BR
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