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Tumor necrosis factor-α induces a kB sequence-specific DNA-binding protein in human hepatoblastoma HepG2 cells

Authors

  • Ranjit Banerjee,

    1. Departments of Neoplastic Diseases, Biochemistry and Microbiology, Mount Sinai School of Medicine of the City University of New York, New York, New York 10029
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  • Saul Karpen,

    1. Departments of Neoplastic Diseases, Biochemistry and Microbiology, Mount Sinai School of Medicine of the City University of New York, New York, New York 10029
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  • Miriam Siekevitz,

    1. Departments of Neoplastic Diseases, Biochemistry and Microbiology, Mount Sinai School of Medicine of the City University of New York, New York, New York 10029
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  • Gabriella Lengyel,

    1. Departments of Neoplastic Diseases, Biochemistry and Microbiology, Mount Sinai School of Medicine of the City University of New York, New York, New York 10029
    Current affiliation:
    1. Second Department of Internal Medicine, Semmelweis University of Medicine, Budapest, Hungary
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  • Joachim Bauer,

    1. Departments of Neoplastic Diseases, Biochemistry and Microbiology, Mount Sinai School of Medicine of the City University of New York, New York, New York 10029
    Current affiliation:
    1. Medizinische Klinik, Labor B13, 7800 Freiburg, Federal Republic of Germany
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  • George Acs M.D.

    Corresponding author
    1. Departments of Neoplastic Diseases, Biochemistry and Microbiology, Mount Sinai School of Medicine of the City University of New York, New York, New York 10029
    • Deparment of Biochemistry, Box 1020, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029—6574
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Abstract

Tumor necrosis factor-α is an inducer of acute-phase protein synthesis in liver cells. The mechanism by which tumor necrosis factor-α alters gene expression in these cells is largely unknown. In this study, we demonstrate that tumor necrosis factor-α 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 (kB) DNA sequences. In contrast to lymphocytic cells where the nuclear factors recognizing the kB sequences are activated by both tumor necrosis factor-α 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-α.

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