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Differential Regulation of Tyrosine Amino-Transferase by Glucocorticoids: Transcriptional and Post-Transcriptional Control

  • E. Brad Thompson
  • P. Gadson
  • G. Wasner
  • S. S. SimonsJr.
Conference paper

Abstract

Current models of steroid hormone action focus on three components: the ligands (steroids) themselves, their receptors, and the cis-active steroid response elements (SRE’s) to which the receptor binds to cause increased or decreased transcriptional activity from nearby genes. Many studies have found that as steroid concentration increases across the range that leads to full occupancy of the receptor, a constant fraction of the steroid-receptor complex becomes more tightly associated with nuclei, presumably interacting with certain SRE’s to effect increasing degrees of response (Baxter et al., 1979). The foundations of these concepts were first established with observations on the induction of tyrosine aminotransferase (E C 2.6.1.5) in HTC cells. This enzyme was one of two that in the late 1950’s had been observed to increase in rat liver in response to glucocorticoid administration (Lin et al., 1957; Lin et al., 1958; Greengard et al.). By establishing a line of liver-derived hepatoma cells (HTC cells), it was possible to resolve clearly several issues not easy to work out in whole animal or whole-organ systems (Thompson et al., 1966). Among these were the fact that in HTC cells, the degree of induction of the transaminase corresponded to the degree of occupancy of the receptor by active glucocorticoids (Baxter et al., 1970; Baxter et al., 1971; Rousseau et al., 1972). This principle was found to hold for a large number of inducible genes, driven by various types of steroids and their receptors.

Keywords

Glucocorticoid Receptor Glutamine Synthetase Mouse Mammary Tumor Virus Tyrosine Aminotransferase Glucocorticoid Response Element 
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Copyright information

© Springer-Verlag New York, Inc. 1989

Authors and Affiliations

  • E. Brad Thompson
  • P. Gadson
  • G. Wasner
  • S. S. SimonsJr.

There are no affiliations available

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