Abstract
Tumor necrosis factor-alpha is an inducer of acute-phase protein synthesis in liver cells. The mechanism by which tumor necrosis factor-alpha alters gene expression in these cells is largely unknown. In this study, we demonstrate that tumor necrosis factor-alpha stimulates human immunodeficiency virus-1 long terminal repeat-promoted gene expression in the human hepatoblastoma HepG2 cell line and increased binding of trans-activating factors to kappa B (kappa B) DNA sequences. In contrast to lymphocytic cells where the nuclear factors recognizing the kappa B sequences are activated by both tumor necrosis factor-alpha and phorbol-12-myristate-13-acetate through a posttranslational mechanism, in HepG2 cells phorbol-12-myristate-13-acetate does not activate these factor(s), and de novo protein synthesis seems to be required in HepG2 cells for gene activation by tumor necrosis factor-alpha.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Base Sequence
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Carcinoma, Hepatocellular / metabolism*
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Chloramphenicol O-Acetyltransferase / genetics
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DNA / genetics
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DNA / metabolism*
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Enhancer Elements, Genetic / genetics
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Gene Expression / drug effects
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Gene Products, tat / pharmacology
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Genes, Viral / genetics
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HIV-1 / genetics
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Humans
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Liver Neoplasms / metabolism*
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Molecular Sequence Data
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NF-kappa B
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Plasmids
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Recombinant Proteins / pharmacology
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Repetitive Sequences, Nucleic Acid
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Tetradecanoylphorbol Acetate / pharmacology
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Trans-Activators / metabolism*
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Transcription Factors / genetics*
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Transfection
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Tumor Cells, Cultured
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Tumor Necrosis Factor-alpha / pharmacology*
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tat Gene Products, Human Immunodeficiency Virus
Substances
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Gene Products, tat
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NF-kappa B
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Recombinant Proteins
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Trans-Activators
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Transcription Factors
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Tumor Necrosis Factor-alpha
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tat Gene Products, Human Immunodeficiency Virus
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DNA
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Chloramphenicol O-Acetyltransferase
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Tetradecanoylphorbol Acetate