Temporary loss of glucocorticoid receptor-mediated regulation of gene expression in heat-shocked cells.
The effect of heat shock on the transcriptional activity of glucocorticoid receptor was assessed using HeLa cells stably transfected with the chloramphenicol acetyltransferase (CAT) gene the transcription of which is controlled by two glucocorticoid-responsive elements placed directly upstream of a core promoter. Heat shock inactivated the high-affinity glucocorticoid binding capacity of the cells and nullified the rate of accumulation of CAT mRNA in the presence of hormone. Hormonal responsiveness was restored on return to normal temperature concomitantly with recovery of high-affinity glucocorticoid binding capacity. Heat inactivation of the receptor was coincident with loss of its solubility and apparently unrelated to receptor degradation.
Mitsiou
D J
DJ
Institute of Biological Research and Biotechnology, National Hellenic Research Foundation, Athens, Greece.
Alexis
M N
MN
D015500:Chloramphenicol O-Acetyltransferase / Q000096:biosynthesis / Q000235:genetics; D003600:Cytosol / Q000378:metabolism; D005786:Gene Expression Regulation; D006367:HeLa Cells; D006358:Hot Temperature; D006801:Humans; D012333:RNA, Messenger / Q000096:biosynthesis; D011965:Receptors, Glucocorticoid / Q000378:metabolism / Q000502:physiology*; D011993:Recombinant Fusion Proteins / Q000096:biosynthesis; D014158:Transcription, Genetic; D015533:Transcriptional Activation / Q000187:drug effects; D014162:Transfection; D014221:Triamcinolone / Q000378:metabolism* / Q000494:pharmacology
D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D011993:Recombinant Fusion Proteins; D014221:Triamcinolone; D015500:Chloramphenicol O-Acetyltransferase