17-11-2014, 03:09 AM
Been looking for this a long time: 
REGULATION OF RECEPTOR NUMBERS
The half-life of steroid hormone receptors ranges from 2 to 4 hours for ERα 4 hours for AR, 7 to 10 hours for PR, and 19 hours for GR. The relatively long half-life of the steroid hormone receptors strongly suggests that the receptor proteins are recycled before eventual degradation.
Steroid hormones generally autoregulate their receptor levels. Desensitization or downregulation of receptor numbers, measured by decreased ligand binding capacity, occurs in response to exposure to high levels of ligand and involves the reduction in receptor mRNA levels, decreasing the number of available receptors. The receptor gene may be negatively regulated by the hormonal ligand itself through its receptor protein interacting with specific HREs in the gene. Upregulation or self-priming may occur in an analogous fashion. Steroid hormones can regulate receptor levels for other hormones (e.g. E2 increases PR levels in estrogen-responsive tissues). Progesterone can downregulate its own receptors, as well as ERα and ERβ. This increase or decrease in receptor levels in homologous or heterologous regulation can be caused by alterations in receptor gene transcription or decay rates for receptor mRNA or protein. Binding of the cytosolic GR complex to very long 3'-untranslated regions of its receptor mRNA has been reported to cause premature degradation.
REGULATION OF RECEPTOR NUMBERS
The half-life of steroid hormone receptors ranges from 2 to 4 hours for ERα 4 hours for AR, 7 to 10 hours for PR, and 19 hours for GR. The relatively long half-life of the steroid hormone receptors strongly suggests that the receptor proteins are recycled before eventual degradation.
Steroid hormones generally autoregulate their receptor levels. Desensitization or downregulation of receptor numbers, measured by decreased ligand binding capacity, occurs in response to exposure to high levels of ligand and involves the reduction in receptor mRNA levels, decreasing the number of available receptors. The receptor gene may be negatively regulated by the hormonal ligand itself through its receptor protein interacting with specific HREs in the gene. Upregulation or self-priming may occur in an analogous fashion. Steroid hormones can regulate receptor levels for other hormones (e.g. E2 increases PR levels in estrogen-responsive tissues). Progesterone can downregulate its own receptors, as well as ERα and ERβ. This increase or decrease in receptor levels in homologous or heterologous regulation can be caused by alterations in receptor gene transcription or decay rates for receptor mRNA or protein. Binding of the cytosolic GR complex to very long 3'-untranslated regions of its receptor mRNA has been reported to cause premature degradation.