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Hyperthermic stress modulates the functions of rat liver glucocorticoid receptor
Author(s) -
Matić Gordana,
Kipić Jasmina,
Ristić Biljana,
Dundjerski Jadranka,
Trajković Divna
Publication year - 1995
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1006/cbir.1995.1063
Subject(s) - glucocorticoid receptor , tyrosine aminotransferase , cytosol , glucocorticoid , endocrinology , medicine , receptor , chemistry , hsp90 , dexamethasone , biology , biochemistry , enzyme , heat shock protein , enzyme inducer , gene
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.