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Intracellular Steroid Receptors

Intracellular steroid receptors, which alter gene expression, exist for corticosteroids, oestrogens and progesterone in the brain, as in the periphery but they cannot account for the relatively rapid depression of CNS function induced by some steroids. This was explained when Harrison and Simmonds (1984) discovered that alphaxalone (the steroid anaesthetic) potentiated the duration of GABA-induced currents at the GABAa receptor in slices of rat cuneate nucleus just like the barbiturates (Fig. 13.6). Of the... [Pg.275]

Figure 17.4 Intracellular steroid receptor activation by hormone ligands, (a) Steroid hormones diffuse across the cell membrane into the cell. (b) Steroid hormone receptors in the basal state bound to accessory proteins, (c) Steroid hormones bind to receptors and accessory proteins are dissociated from the receptors. (d) Hormone receptor complexes dimerize. (e) Dimer complexes enter the nucleus and initiate transcription of responsive genes. Figure 17.4 Intracellular steroid receptor activation by hormone ligands, (a) Steroid hormones diffuse across the cell membrane into the cell. (b) Steroid hormone receptors in the basal state bound to accessory proteins, (c) Steroid hormones bind to receptors and accessory proteins are dissociated from the receptors. (d) Hormone receptor complexes dimerize. (e) Dimer complexes enter the nucleus and initiate transcription of responsive genes.
The mechanisms of action of steroid hormones on lymphoid, mammary, and prostatic cancer have been partially clarified. Specific cell surface receptors have been identified for estrogen, progesterone, corticosteroids, and androgens in neoplastic cells in these tissues. As in normal cells, steroid hormones also form an intracellular steroid-receptor complex that ultimately binds directly to nuclear proteins associated with DNA to activate transcription of a broad range of cellular genes involved in cell growth and proliferation (see Chapter 39 Adrenocorticosteroids Adrenocortical Antagonists). [Pg.1304]

DNA. Steroid receptors have been reported in mitochondria (17) and cell membranes, although it is not yet clear whether all of these receptors are the same as the intracellular steroid receptors (16, 18-22 vs. 23). Some of the membrane-bound receptors for steroids are G protein-coupled receptors (24—27). A recent report suggests that membrane-bound steroid receptors can interact with, and augment the transcriptional activity of, the intracellular receptors (24). Finally, steroids can bind to nonreceptor molecules such as enzymes and transport proteins (see above), which may have yet undiscovered consequences. [Pg.1734]

A. Corticosteroids As indicated in Figure 18-1, corticosteroids inhibit the production of arachidonic acid by phospholipases in the membrane. This effect is mediated by intracellular steroid receptors that, when activated by an appropriate steroid, increase expression of specific proteins capable of inhibiting phospholipase. Steroids also inhibit the synthesis of COX-2. These actions are thought to be the major mechanisms of the important anti-inflammatory action of corticosteroids. [Pg.176]

The main endogenous mineralocorticoid is aldosterone, which is mainly produced by the outer layer of the adrenal medulla, the zonaglomerulosa. Aldostorone, like other steroids, binds to a specific intracellular (nuclear) receptor, the mineralocorticoid receptor (MR). Its main action is to increase sodium reabsotption by an action on the distal tubules in the kidney, which is accompanied by an increased excretion of potassium and hydrogen ions. [Pg.775]

Most receptors (a notable exception being the steroid receptors that influence DNA transcription) are located on the cell surface, and purified cell membranes are thus an obvious choice of preparation. When a tissue is homogenized, however, any membrane fraction isolated may well contain membranes from intracellular organelles in addition to cell membranes from all the cell types present in the tissue. Thus, brain membranes will contain membranes not only from neurons but... [Pg.166]

Understanding of the intracellular localization of steroid receptors has gone through a number of phases, beginning with the view that receptors translocated from cytoplasm to nucleus in the presence of hormone. Indeed, with the exception of thyroid hormone receptors, which are exclusively nuclear in location, cell fractionation studies have revealed that in the absence of hormone, steroid receptors are extracted in the soluble or cytosolic fraction. However, when steroid is present in the cell, many occupied receptors are retained by purified cell nuclei. Histological procedures, such as immunocytochemistry, have confirmed the largely nuclear localization of occupied receptors, but... [Pg.851]

Cortisol secreted in response to stress, is permissive for glucagon in hypoglycemia and acts through an intracellular receptor, which, like other steroid receptors, is a zinc-finger DNA binding protein,... [Pg.74]

H)2D3 exerts its influence within target tissues through high-affinity sterol-specific intracellular receptor proteins. The D3 receptor, similar to steroid receptor systems, translocates the hormone from the cell cytoplasm to the nucleus, where biological response is initiated via transcription and translation (Fig. 66.3). [Pg.758]

Ginsenosides belong to a family of steroids and share their structural characteristics. They can traverse cell membranes freely similar to steroids. Moreover, their presence has been demonstrated within cells, particularly the nucleus. Steroid hormone action, steroids that bind nuclear receptors, are thought to affect primarily the transcription of mRNA and subsequent protein synthesis. Intracellular steroid-binding proteins present possible attractive targets for ginsenosides. [Pg.371]

Steroid hormones achieve their effects on target tissues through intracellular receptor proteins. According to recent views, oestrogen and progestin receptors are localized in the nuclear compartment of the cells, whereas glucocorticoid receptors may reside in both the cytoplasm and the nucleus. Determination of the intracellular localization of androgen receptors awaits the development of (monoclonal) antibodies which will enable immunohistochemical studies. The molecular aspects of the mechanism of action of steroid hormones will be covered in other chapters [1-3] in this volume. The present chapter deals with the characterization, assay and purification of steroid receptors. [Pg.49]

Whether unoccupied GR are totally nuclear is less clear. Immunocytochemical studies with anti-GR antibodies show both cytoplasmic and nuclear localization at the light level, and an increase in nuclear staining simultaneous with decreased cytoplasmic staining in response to addition of glucocorticoids [106-109]. It may well be that GR have a different intracellular distribution from the sex-steroid receptors. [Pg.256]

Betamethasone is a corticosteroid. Corticosteroids are very lipophilic (due to their hydrocarbon skeleton) and as a result can passively diffuse into target cells. It acts by binding to the intracellular corticosteroid receptor protein, which is found within the cytosol. The resulting complex translocates to the nucleus and induces synthesis of mediator proteins (e.g. metabolic enzymes and lipocortin). The binding of steroid hormones to their receptors causes changes in gene transcription and cell function. Corticosteroids reduce the inflammatory reaction by limiting capillary dilatation and vascular permeability. [Pg.311]

Some ligands do not interact principally with cell surface receptors, but diffuse into cells and bind to intracellular receptors in the cytoplasm. For example, ligand binding to cytoplasmic steroid receptors initiates a process that is not well understood but that involves the movement of steroid-bound receptor into the cell nucleus, where the receptor molecule interacts with genomic material, resulting in alterations in gene expression and protein synthesis. [Pg.362]


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