The Agamma-195 (c-->g) Mutation In Hereditary Persistence Of Fetal Hemoglobin Is Not Associated With Activation Of A Reporter Gene In Vitro.

dc.creatorSchreiber, R
dc.creatorGonçalves, M S
dc.creatorJunqueira, M L
dc.creatorSaad, S T
dc.creatorKrieger, J E
dc.creatorCosta, F F
dc.date2001-Apr
dc.date2015-11-27T12:29:14Z
dc.date2015-11-27T12:29:14Z
dc.date.accessioned2018-03-29T00:55:51Z
dc.date.available2018-03-29T00:55:51Z
dc.identifierBrazilian Journal Of Medical And Biological Research = Revista Brasileira De Pesquisas Médicas E Biológicas / Sociedade Brasileira De Biofísica ... [et Al.]. v. 34, n. 4, p. 489-92, 2001-Apr.
dc.identifier0100-879X
dc.identifier
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/11285460
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/194974
dc.identifier11285460
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1295207
dc.descriptionHereditary persistence of fetal hemoglobin is an uncommon, benign disorder in which the expression of gamma-globin genes persists into adult life. Several point mutations have been associated with the increased gamma-globin gene promoter activity. We evaluated the -195 (C-->G) mutation by a functional in vitro assay based on the luciferase reporter gene system. The results indicated that the increased promoter activity observed in vivo could not be reproduced in vitro under the conditions employed, suggesting that other factors may be involved in the overexpression of the gamma-globin gene containing the -195 (C-->G) mutation. Furthermore, this is the first time that the -195 (C-->G) mutation of the Agamma-globin gene has been evaluated by in vitro gene expression.
dc.description34
dc.description489-92
dc.languageeng
dc.relationBrazilian Journal Of Medical And Biological Research = Revista Brasileira De Pesquisas Médicas E Biológicas / Sociedade Brasileira De Biofísica ... [et Al.]
dc.relationBraz. J. Med. Biol. Res.
dc.rightsaberto
dc.rights
dc.sourcePubMed
dc.subjectAdult
dc.subjectDna Primers
dc.subjectFetal Hemoglobin
dc.subjectGene Expression
dc.subjectGenes, Reporter
dc.subjectGlobins
dc.subjectHemoglobinopathies
dc.subjectHumans
dc.subjectLuciferases
dc.subjectMutation
dc.subjectPoint Mutation
dc.subjectPolymerase Chain Reaction
dc.subjectTransfection
dc.subjectBeta-galactosidase
dc.titleThe Agamma-195 (c-->g) Mutation In Hereditary Persistence Of Fetal Hemoglobin Is Not Associated With Activation Of A Reporter Gene In Vitro.
dc.typeArtículos de revistas


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