Please use this identifier to cite or link to this item:
|Type:||Artigo de periódico|
|Title:||Human T-celllymphotropic Virus Type L Transac1tvator Tax And Transcription Factor Sp1 Interact On The Gata3 Promoter|
|Abstract:||Human T cell leukemia virus type I (HTLV I) is a causative agent of adult T-cell leukemia and the HTLV I associated myelopathy or tropical spastic paraparesis. Although the infection has been reported in every region of the world, moderate-to-high rates of the infection can be found in South America. The majority of seropositive individuals (over 95%) remains asymptomatic. The causes of disease progression are unknown but might involve genetic predisposition, different viral strain and differences in the host immune response. Several lines of evidence suggest that the Tax protein, a 40-kDa transcriptional viral activator, is critical for HTLV-I gene regulation and virus-induced cellular transformation. It seems that several events in HTLV I infected cells are required for the development of the full malignant phenotype. GATA3 is a specific T cell transcription factor , functionally important in the regulation of multiple T-cell specific genes. This transcription factor is an essential and specific regulator of early thymocyte development and is downregulated in HTLVI infection. In order to characterize the relationship between Tax protein and the GATA3 transcription factor, we studied, by Eletrophoretic Mobility Shift Assay (EMSA), the potential interaction of Tax with the GATA3 promoter. The purified Tax protein and anti-Tax antiserum were kindly provided by Dr. Susan J. Marriott. The recombinant human Spl was obtained from Promega (Madison, WI). Our results demonstrated that Tax binds to the GATA3 promoter through the transcription factor Spl. Competition studies showed that the complex formation was specific and supershift analysis demonstrated that Tax was involved in this formation. However, in the absence of Tax, Sp 1 does not bind to the GATA3 promoter. Tax might play a role in early leukemogenesis by expanding the pool of proliferating T cells and thereby creating the condition for subsequent events that lead to T cell malignancy. Therefore, the results here presented may be an important contribution to elucidate the oncogenic potential of Tax protein.|
|Appears in Collections:||Unicamp - Artigos e Outros Documentos|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.