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  • Title: Steroid hormone receptors and mechanism of action.
    Journal: Res Reprod; 1977 Nov; 9(6):2-4. PubMed ID: 12299912.
    Abstract:
    The 1st step in the action of a steroid hormone involves entering a target cell where it is recognized and bound by a soluble macromolecule called a cytosol receptor (Re) specific for that hormone. The receptor hormone complex (ReS) is translocated to the cell's nucleus (RnS) where it binds to a large number of sites on chromatin. The binding of RnS to acceptor sites is thought to make gene sites available for transcription by RNA polymerase which subsequently results in elevated cellular RNA and protein synthesis. The 3-H steroid exchange assay based on the temperature dependence of the rate of steroid dissociation can be used to differentiate occupied and unoccupied receptors. The method has been used to examine the relationship between nuclear binding of the Rn estradiol complex and the stimulation of growth processes in the rat uterus. A single injection of .2 mcg/100 g body weight of estradiol causes the nuclear accumulation and retention of approximately 10-20% of the total number of uterine Re sites. Nuclear occupancy for 6 or more hours appears to be a requirement for stimulation of late uterotrophic events such as DNA synthesis, sustained stimulation of RNA polymerase activities, and cellular hypertrophy and hyperplasia. Estriol, a short-acting estrogen, has been classified as a weak estrogen, but it acts as such only when administered in a single injection, in which case it stimulates all early uterotrophic events but does not stimulate significant uterine growth. When estriol is present in a continuous fashion it is a highly effective estrogen. Longterm nuclear retention of the RnE complexes is necessary for uterine hypertrophy and hyperplasia. RnE complexes appear to interact with the genome to open gene sites for transcription; continued transcriptional activity is required for full uterine growth. Nonsteroidal estrogen antagonists have estrogen properties in some cells but act as estrogen antagonists in others. Progesterone appears to modify or redirect estrogen action by modulating estrogen receptor levels. Progesterone may act by reducing the level of available cytoplasmic estrogen receptors and hence decreasing the likelihood of receptor binding or by interfering with the nuclear retention of the RnE complex and decreasing the ability of these complexes to stimulate transcriptional events.
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