Human T-cell leukemia virus type I tax protein induces the expression of anti-apoptotic gene Bcl-xL in human T-cells through nuclear factor-kappaB and c-AMP responsive element binding protein pathways.
Constitutive expression of Lewis X in these cells is due to the transcriptional activation of Fuc-T VII, the rate-limiting enzyme in the sialyl Lewis X synthesis, induced by the Tax protein encoded by the human T-cell leukemia virus-1, the etiological virus for this leukemia.
First, a premature stop codon in the 5' half of the tax gene that looses transactivation activity on the viral enhancer was observed in 3 patients with acute and 1 patient with chronic ATL.
We investigated the T-cell receptor (TCR) repertoire of CD8(+) T cells that recognize the Tax11-19 immunodominant epitope of Tax protein expressed by human T-cell leukemia virus (HTLV-1) that is implicated in the disease HTLV-1-associated myelopathy (HAM/TSP).
Invasion of rat fibroblastic cells Rat-1 through Matrigel was shown to be promoted by transfection with tax gene of human T-cell leukemia virus type 1.
Cytokine expression and tumorigenicity of large granular lymphocytic leukemia cells from mice transgenic for the tax gene of human T-cell leukemia virus type I.
To determine the effect of the human T cell leukemia virus type I (HTLV-I) tax gene on interleukin-6 (IL-6) production and gene transcription in synovial cells, we established the synovial cell line, E-11, from a patient with rheumatoid arthritis.
Peripheral blood T cells were immortalized in vitro by introduction of the Tax1 gene of human T-cell leukemia virus type 1 (HTLV-1) with a retroviral vector and were characterized for transformation-associated markers.