On the mechanism of estrogen receptor replenishment: recycling, resynthesis and/or processing.
Estrogen receptor replenishment has been extensively studied after a single injection of estradiol-17 beta in the rat. Most studies indicate that replenishment, under these conditions, is due both to recycling and to resynthesis of receptor. In the case of short-acting estrogens, total replenishment occurs in the absence of protein synthesis and loss of nuclear receptor closely corresponds to an increase in cytoplasmic receptor. After estradiol-17 beta injection, there is a loss of nuclear receptor without a corresponding increase in cytoplasmic receptor, leading to a loss in total receptor content or 'processing'. Since little processing occurs with the active, short-acting estrogen, we propose that processing is not essential for estrogen action. Evidence is accumulating to indicate that processing may be due to a reversible inactivation of the steroid binding capacity of the receptor. We discuss a model in which there are two routes for replenishment: a simple equilibrium scheme where no processing occurs and a second route where the receptor is processed to a form with low affinity for estrogen which must be reactivated before binding can occur.
D000818:Animals; D002467:Cell Nucleus / Q000378:metabolism; D003593:Cytoplasm / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology; D008954:Models, Biological; D051381:Rats; D011960:Receptors, Estrogen / Q000378:metabolism*; D013997:Time Factors
D011960:Receptors, Estrogen; D004958:Estradiol