Characteristics and Specificity of the Glucocorticoid “Carrier” of Rat Liver Plasma Membrane
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The physiological action of steroid hormones in a target cell is assumed to be initiated, primarily, by the binding of the hormone to specific intracellular “receptor” proteins.1 Following this interaction the hormone-receptor complex is activated by agents such as the H+-ion concentration, cations and temperature; the activated form then crosses the nuclear membrane to react with DNA in the nucleus. The synthesis of m-RNA and of specific protein(s) characteristic of the particular tissue is the result of the series of events.1–4 In order to set these events inside the cell into motion the fraction of the steroid which is present in the free form in the blood, must cross the plasma membrane to enter the cell. Study of the entry has been the subject of investigation by many authors; mediated and non-mediated modes of entry have been postulated (for reviews see Refs. 5 and 6). Some probable reasons for the divergent views may be that a), depending on the steroid, the tissue or the cell, and the methodology used to study entry, influx might occur extremely rapidly making such measurement impossible or inaccurate; b) the concentration of steroids used do not bear correlation with the concentration of free steroids in blood, with the result that a non-mediated process of entry predominates and the existence of a mediated process of entry is readily overlooked. The former may be the preferred process in certain cells for some hormones. c) A factor of utmost importance in studies on the entry of hormones into cells, is the inability to distinguish between the process of entry and the binding of the steroid to intracellular components. Despite these difficulties there is increasing evidence supporting membrane-mediated processes in the entry of several hormones (for reviews see Refs. 5 and 7).
KeywordsSpecific Uptake Plasma Membrane Vesicle Hormone Transport Cytoplasmic Receptor Intact Hepatocyte
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