Abstract
Human T-cell leukemia virus type 1 is an oncogenic retrovirus etiologically causal of adult T-cell leukemia. The virus encodes a Tax oncoprotein, which functions in transcriptional regulation, cell cycle control, and transformation. Because adult T-cell leukemia is a highly virulent cancer that is resistant to numerous chemotherapeutic treatments, to understand better this disease it is important to comprehend how human T-cell leukemia virus type 1 promotes cellular growth and survival. Most of the existing data point to Tax activation of NF-kappaB as important for cellular proliferation and transformation. We show here that Tax, in the absence of NF-kappaB signaling, can activate activator protein-1 to promote cellular proliferation and survival. Tax is shown to activate activator protein-1 through the phosphatidylinositol 3-kinase/Akt pathway.
Publication types
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Research Support, N.I.H., Intramural
MeSH terms
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Animals
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Cell Line, Transformed
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Cell Proliferation*
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Cell Transformation, Viral
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Cells, Cultured
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Chlorocebus aethiops
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Fibroblasts / metabolism
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Fibroblasts / virology
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Gene Expression Regulation, Viral
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Gene Products, tax / genetics
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Gene Products, tax / metabolism
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Gene Products, tax / physiology*
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Genes, Reporter
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Human T-lymphotropic virus 1 / physiology*
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Humans
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Jurkat Cells
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Luciferases / metabolism
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Mice
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Phosphatidylinositol 3-Kinases / metabolism
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Proto-Oncogene Proteins c-akt / analysis
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Proto-Oncogene Proteins c-akt / metabolism
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Proto-Oncogene Proteins c-akt / physiology*
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T-Lymphocytes / metabolism
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T-Lymphocytes / virology
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Transcription Factor AP-1 / metabolism
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Transcription Factor AP-1 / physiology*
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Vero Cells
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beta-Galactosidase / analysis
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beta-Galactosidase / metabolism
Substances
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Gene Products, tax
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Transcription Factor AP-1
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Luciferases
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Proto-Oncogene Proteins c-akt
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beta-Galactosidase