Hyperthermic stress modulates the functions of rat liver glucocorticoid receptor

Authors

  • Gordana Matić,

    Corresponding author
    1. Department of Biochemistry and Molecular Biology, Institute for Biological Research, 29. Novembra 142, 11060 Belgrade, Yugoslavia
      Department of Biochemistry and Molecular Biology, Institute for Biological Research, 29. Novembra 142, 11060 Belgrade, Yugoslavia
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  • Jasmina Kipić,

    1. Department of Biochemistry and Molecular Biology, Institute for Biological Research, 29. Novembra 142, 11060 Belgrade, Yugoslavia
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  • Biljana Ristić,

    1. Department of Biochemistry and Molecular Biology, Institute for Biological Research, 29. Novembra 142, 11060 Belgrade, Yugoslavia
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  • Jadranka Dundjerski,

    1. Department of Ecology, Institute for Biological Research, 29. Novembra 142, 11060 Belgrade, Yugoslavia
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  • Divna Trajković

    1. Department of Biochemistry and Molecular Biology, Institute for Biological Research, 29. Novembra 142, 11060 Belgrade, Yugoslavia
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Department of Biochemistry and Molecular Biology, Institute for Biological Research, 29. Novembra 142, 11060 Belgrade, Yugoslavia

ABSTRACT

A mild whole body hyperthermic stress causes a rapid and reversible reduction of rat liver glucocorticoid receptor (GR) binding capacity and affects the stability of the GR-DNA complexes formed after thermal transformation of the receptor. These changes appear to be physiologically relevant, since they are accompanied by a decrease in dexamethasone induction of hepatic tyrosine aminotransferase (TAT). In spite of the decreased rate of the GR degradation in liver cytosol of hyperthermic as compared to control rats, the total amount of the GR and its proteolytic products recognized by BuGR2 monoclonal antibody was found to be lower in the former cytosol, but higher in the respective nuclei.

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