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HYPERTHERMIC STRESS AFFECTS GLUCOCORTICOID RECEPTOR‐MEDIATED TRANSCRIPTION IN RAT LIVER
Author(s) -
VIDOVIĆ STOJKO,
ČVORO ALEKSANDRA,
DUNDJERSKI JADRANKA,
TRAJKOVIĆ DIVNA,
MATIĆ GORDANA
Publication year - 1996
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.1996.0072
Subject(s) - glucocorticoid receptor , tyrosine aminotransferase , glucocorticoid , cytosol , transcription factor , medicine , cytoplasm , nuclear receptor , endocrinology , stimulation , transcription (linguistics) , receptor , biology , chemistry , microbiology and biotechnology , gene , biochemistry , enzyme , enzyme inducer , linguistics , philosophy
Binding capacity of the cytoplasmic and nuclear glucocorticoid receptor (GR) and the activity of tyrosine aminotransferase (TAT) were examined in the liver of intact and adrenalectomized rats exposed to 41°C whole body hyperthermic stress. In glucocorticoid‐deprived animals, stress‐induced decrease in the cytoplasmic steroid binding was followed by parallel increases in its nuclear binding and TAT activity, suggesting a stimulation of TAT gene transcription by the GR in the absence of the ligand. In intact animals, however, a diminution of the steroid binding in the cytosol, its unchanged nuclear binding and an impairment of TAT activity were observed upon the stress. The results imply that stress could elicit different structural or functional alterations of unliganded vs liganded GR.