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Virology ; 443(2): 226-35, 2013 Sep 01.
Article in English | MEDLINE | ID: mdl-23791017

ABSTRACT

Human T-cell leukemia virus type 1 (HTLV-1) Tax (Tax1) plays crucial roles in leukemogenesis in part through activation of NF-κB. In this study, we demonstrated that Tax1 activated an NF-κB binding (gpκB) site of the gp34/OX40 ligand gene in a cell type-dependent manner. Our examination showed that the gpκΒ site and authentic NF-κB (IgκB) site were activated by Tax1 in hematopoietic cell lines. Non-hematopoietic cell lines including hepatoma and fibroblast cell lines were not permissive to Tax1-mediated activation of the gpκB site, while the IgκB site was activated in those cells in association with binding of RelB. However RelA binding was not observed in the gpκB and IgκB sites. Our results suggest that HTLV-1 Tax1 fails to activate the canonical pathway of NF-κB in non-hematopoietic cell lines. Cell type-dependent activation of NF-κB by Tax1 could be associated with pathogenesis by HTLV-1 infection.


Subject(s)
Gene Products, tax/metabolism , Human T-lymphotropic virus 1/pathogenicity , Lymphocytes/virology , NF-kappa B/metabolism , Transcriptional Activation , Cell Line , HeLa Cells , Human T-lymphotropic virus 1/genetics , Human T-lymphotropic virus 1/metabolism , Humans , Jurkat Cells , NF-kappa B/chemistry , NF-kappa B/genetics , OX40 Ligand/genetics , OX40 Ligand/metabolism , Promoter Regions, Genetic , Receptors, OX40/genetics , Receptors, OX40/metabolism , Transcription Factor RelA/genetics , Transcription Factor RelA/metabolism
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