Journal articles on the topic 'Steroid receptors'
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1
Baker, ME. "Recent insights into the origins of adrenal and sex steroid receptors." Journal of Molecular Endocrinology 28, no. 3 (June 1, 2002): 149–52. http://dx.doi.org/10.1677/jme.0.0280149.
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The recent cloning by Thornton (2001) of estrogen, progesterone and corticoid receptors from lamprey provides important insights into the early evolution of adrenal and sex steroid receptors and an opportunity to elucidate the ancient steroids that regulated gene transcription. Inclusion of lamprey sequences in a steroid receptor phylogeny indicates that the estrogen receptor is the most ancient of these receptors, followed by the progesterone receptor and the corticoid receptor. Thornton proposed that estradiol was the earliest of the steroids to activate a steroid receptor. An alternative hypothesis is that a steroid in the Delta(5) pathway activated the ancestral estrogen receptor.
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Baker, ME. "Adrenal and sex steroid receptor evolution: environmental implications." Journal of Molecular Endocrinology 26, no. 2 (April 1, 2001): 119–25. http://dx.doi.org/10.1677/jme.0.0260119.
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The nuclear receptor family responds to a diverse group of ligands, including steroids, retinoids, thyroid hormone, prostaglandins and fatty acids. Previous sequence analyses of adrenal and sex steroid receptors indicate that they form a clade separate from other nuclear receptors. However, the relationships of adrenal and sex steroid receptors to each other and to their ancestors are not fully understood. We have used new information from androgen, estrogen, mineralocorticoid and progesterone receptors in fish to better resolve the phylogeny of adrenal and sex steroid receptors. Sequence divergence between fish and mammalian steroid receptors correlates with differences in steroid specificity, suggesting that phylogeny needs to be considered in evaluating the endocrine effects of xenobiotics. Among the vertebrate steroid receptors, the most ancient is the estrogen receptor. The phylogeny indicates that adrenal and sex steroid receptors arose in a jawless fish or a protochordate and that changes in the sequence of the hormone-binding domain have slowed considerably in land vertebrates. The retinoid X receptor clade is closest to the adrenal and sex steroid receptor clade. Retinoid X receptor is noteworthy for its ability to form dimers with other nuclear receptors, an important mechanism for regulating the action of retinoid X receptor and its dimerization partners. In contrast, the adrenal and sex steroid receptors bind to DNA as homodimers. Moreover, unliganded adrenal and sex steroid receptors form complexes with heat shock protein 90. Thus, the evolution of adrenal and sex steroid receptors involved changes in protein-protein interactions as well as ligand recognition.
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Marcinkowska, Ewa, and Antoni Wiedłocha. "Steroid signal transduction activated at the cell membrane: from plants to animals." Acta Biochimica Polonica 49, no. 3 (September 30, 2002): 735–45. http://dx.doi.org/10.18388/abp.2002_3782.
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Steroid hormones in plants and in animals are very important for physiological and developmental regulation. In animals steroid hormones are recognized by nuclear receptors, which transcriptionally regulate specific target genes following binding of the ligand. In addition, numerous rapid effects generated by steroids appear to be mediated by a mechanism not depending on the activation of nuclear receptors. Although the existence of separate membrane receptors was postulated many years ago and hundreds of reports supporting this hypothesis have been published, no animal membrane steroid receptor has been cloned to date. Meanwhile, a plant steroid receptor from Arabidopsis thaliana has been identified and cloned. It is a transmembrane protein which specifically recognizes plant steroids (brassinosteroids) at the cell surface and has a serine/threonine protein kinase activity. It seems that plants have no intracellular steroid receptors, since there are no genes homologous to the family of animal nuclear steroid receptors in the genome of A. thaliana. Since the reason of the rapid responses to steroid hormones in animal cells still remains obscure we show in this article two possible explanations of this phenomenon. Using 1,25-dihydroxyvitamin D(3) as an example of animal steroid hormone, we review results of our and of other groups concordant with the hypothesis of membrane steroid receptors. We also review the results of experiments performed with ovarian hormones, that led their authors to the hypothesis explaining rapid steroid actions without distinct membrane steroid receptors. Finally, examples of polypeptide growth factor that similarly to steroids exhibit a dual mode of action, activating not only cell surface receptors, but also intracellular targets, are discussed.
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Wiseman, Helen, and Rosanna Duffy. "Steroids, steroid receptors and disease." Trends in Molecular Medicine 7, no. 4 (April 2001): 146–47. http://dx.doi.org/10.1016/s1471-4914(01)01978-5.
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Hammes, Stephen R., and Ellis R. Levin. "Extranuclear Steroid Receptors: Nature and Actions." Endocrine Reviews 28, no. 7 (October 4, 2007): 726–41. http://dx.doi.org/10.1210/er.2007-0022.
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Rapid effects of steroid hormones result from the actions of specific receptors localized most often to the plasma membrane. Fast-acting membrane-initiated steroid signaling (MISS) 1leads to the modification of existing proteins and cell behaviors. Rapid steroid-triggered signaling through calcium, amine release, and kinase activation also impacts the regulation of gene expression by steroids, sometimes requiring integration with nuclear steroid receptor function. In this and other ways, the integration of all steroid actions in the cell coordinates outcomes such as cell fate, proliferation, differentiation, and migration. The nature of the receptors is of intense interest, and significant data suggest that extranuclear and nuclear steroid receptor pools are the same proteins. Insights regarding the structural determinants for membrane localization and function, as well as the nature of interactions with G proteins and other signaling molecules in confined areas of the membrane, have led to a fuller understanding of how steroid receptors effect rapid actions. Increasingly, the relevance of rapid signaling for the in vivo functions of steroid hormones has been established. Examples include steroid effects on reproductive organ development and function, cardiovascular responsiveness, and cancer biology. However, although great strides have been made, much remains to be understood concerning the integration of extranuclear and nuclear receptor functions to organ biology. In this review, we highlight the significant progress that has been made in these areas.
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Adcock, I. M., S. J. Lane, C. R. Brown, M. J. Peters, T. H. Lee, and P. J. Barnes. "Differences in binding of glucocorticoid receptor to DNA in steroid-resistant asthma." Journal of Immunology 154, no. 7 (April 1, 1995): 3500–3505. http://dx.doi.org/10.4049/jimmunol.154.7.3500.
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Abstract Although glucocorticosteroids are a very effective treatment for asthma and other chronic inflammatory diseases, a small proportion of patients are resistant to their therapeutic effects. The molecular mechanism for this steroid resistance is unclear. Steroid resistance cannot be explained by pharmacokinetic mechanisms, by a defect in the binding of steroids to glucocorticoid receptors, nor by defective nuclear translocation of this receptor, thereby suggesting that the molecular abnormality lies distal to nuclear translocation. We examined the ability of nuclear translocated glucocorticoid receptors to bind to their DNA binding sites (GRE) using electrophoretic mobility shift assays in PBMC from patients with steroid-sensitive and steroid-resistant asthma. The binding of the glucocorticoid receptor to DNA in these patients was also studied using Scatchard analysis. Dexamethasone induced a significant rapid and sustained twofold increase in GRE binding in PBMCs from steroid-sensitive asthmatic patients and nonasthmatic individuals, but this was markedly reduced in steroid-resistant asthmatic patients. Scatchard analysis of glucocorticoid receptor-GRE binding showed no change in binding affinity but did show a reduced number of receptors available for DNA binding in the steroid-resistant patients. These results suggest that the ability of the glucocorticoid receptor to bind to GRE is impaired in steroid-resistant patients because of a reduced number of receptors available for binding to DNA.
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Godowski, Paul J., and Didier Picard. "Steroid receptors." Biochemical Pharmacology 38, no. 19 (October 1989): 3135–43. http://dx.doi.org/10.1016/0006-2952(89)90605-9.
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Levin, Ellis R. "Extranuclear estrogen receptor's roles in physiology: lessons from mouse models." American Journal of Physiology-Endocrinology and Metabolism 307, no. 2 (July 15, 2014): E133—E140. http://dx.doi.org/10.1152/ajpendo.00626.2013.
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Steroid receptors exist and function in multiple compartments of cells in most organs. Although the functions and nature of some of these receptors is being defined, important aspects of receptor localization and signaling to physiology and pathophysiology have been identified. In particular, extranuclear sex steroid receptors have been found in many normal cells and in epithelial tumors, where they enact signal transduction that impacts both nongenomic and genomic functions. Here, I focus on the progress made in understanding the roles of extranuclear estrogen receptors (ER) in physiology and pathophysiology. Extranuclear ER serve as a model to selectively intervene with novel receptor reagents to prevent or limit disease progression. Recent novel mouse models and membrane ER-selective agonists also provide a better understanding of receptor pool cross-talk that results in the overall integrative actions of sex steroids.
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Mukudai, Shigeyuki, Ken Ichi Matsuda, Takeshi Nishio, Yoichiro Sugiyama, Hideki Bando, Ryuichi Hirota, Hirofumi Sakaguchi, Yasuo Hisa, and Mitsuhiro Kawata. "Differential Responses to Steroid Hormones in Fibroblasts From the Vocal Fold, Trachea, and Esophagus." Endocrinology 156, no. 3 (March 1, 2015): 1000–1009. http://dx.doi.org/10.1210/en.2014-1605.
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Abstract There is accumulating evidence that fibroblasts are target cells for steroids such as sex hormones and corticoids. The characteristics of fibroblasts vary among tissues and organs. Our aim in this study is to examine differences in responses to steroid hormones among fibroblasts from different cervicothoracic regions. We compared the actions of steroid hormones on cultured fibroblasts from the vocal folds, which are considered to be the primary target of steroid hormones, and the trachea and esophagus in adult male rats. Expression of steroid hormone receptors (androgen receptor, estrogen receptor α, and glucocorticoid receptor) was identified by immunofluorescence histochemistry. Androgen receptor was much more frequently expressed in fibroblasts from the vocal fold than in those from the trachea and esophagus. Cell proliferation analysis showed that administration of testosterone, estradiol, or corticosterone suppressed growth of all 3 types of fibroblasts. However, mRNA expression for extracellular matrix–associated genes, including procollagen I and III and elastin, and hyaluronic acid synthase I was elevated only by addition of testosterone to fibroblasts from the vocal fold. These results indicate that each steroid hormone exerts region-specific effects on cervicothoracic fibroblasts with different properties through binding to specific receptors.
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Plese, J. P. P., V. R. Martins, M. T. P. Lopes, and M. M. Brentani. "Steroid receptors in meningiomas." Arquivos de Neuro-Psiquiatria 43, no. 4 (December 1985): 365–71. http://dx.doi.org/10.1590/s0004-282x1985000400005.
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Cytosolic estrogen (ER), progesterone (PR), androgen (AR) and glucocorticoid receptors (GR) were evaluated in 10 meningiomas using a dextran charcoal coated method. We consider as positive specific receptor values >10fMol/mg protein. In this study 20% of the meningiomas contained very low titers of specific ER. PR was detectable in 90% of the tumors, at high levels. The mean PR content of PR+ tumors was 60±38fMol/mg prot. GR and AR were present in moderate levels, in 70% of the tumors. Competition studies demonstrated steroid specificity for these hormone-binding proteins. Female patients have a higher receptor incidence and titer. In conclusion, it can be hypothesized that the meningioma are a target tissue for steroids and that endocrine therapy may be relevant to unoperable and/or reccurent tumors.
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Knutti, Darko, Adesh Kaul, and Anastasia Kralli. "A Tissue-Specific Coactivator of Steroid Receptors, Identified in a Functional Genetic Screen." Molecular and Cellular Biology 20, no. 7 (April 1, 2000): 2411–22. http://dx.doi.org/10.1128/mcb.20.7.2411-2422.2000.
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ABSTRACT Steroid receptors mediate responses to lipophilic hormones in a tissue- and ligand-specific manner. To identify nonreceptor proteins that confer specificity or regulate steroid signaling, we screened a human cDNA library in a steroid-responsive yeast strain. One of the identified cDNAs, isolated in the screen as ligand effect modulator 6, showed no homology to yeast or Caenorhabditis elegansproteins but high similarity to the recently described mouse coactivator PGC-1 and was accordingly termed hPGC-1. The hPGC-1 DNA encodes a nuclear protein that is expressed in a tissue-specific manner and carries novel motifs for transcriptional regulators. The expression of hPGC-1 in mammalian cells enhanced potently the transcriptional response to several steroids in a receptor-specific manner. hPGC-1-mediated enhancement required the receptor hormone-binding domain and was dependent on agonist ligands. Functional analysis of hPGC-1 revealed two domains that interact with steroid receptors in a hormone-dependent manner, a potent transcriptional activation function, and a putative dimerization domain. Our findings suggest a regulatory function for hPGC-1 as a tissue-specific coactivator for a subset of nuclear receptors.
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Simoncini, T., and AR Genazzani. "Non-genomic actions of sex steroid hormones." European Journal of Endocrinology 148, no. 3 (March 1, 2003): 281–92. http://dx.doi.org/10.1530/eje.0.1480281.
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Steroid hormone receptors have been traditionally considered to act via the regulation of transcriptional processes, involving nuclear translocation and binding to specific response elements, and ultimately leading to regulation of gene expression. However, novel non-transcriptional mechanisms of signal transduction through steroid hormone receptors have been identified. These so-called 'non-genomic' effects do not depend on gene transcription or protein synthesis and involve steroid-induced modulation of cytoplasmic or cell membrane-bound regulatory proteins. Several relevant biological actions of steroids have been associated with this kind of signaling. Ubiquitous regulatory cascades such as mitogen-activated protein kinases, the phosphatidylinositol 3-OH kinase and tyrosine kinases are modulated through non-transcriptional mechanisms by steroid hormones. Furthermore, steroid hormone receptor modulation of cell membrane-associated molecules such as ion channels and G-protein-coupled receptors has been shown. TIssues traditionally considered as 'non-targets' for classical steroid actions are instead found to be vividly regulated by non-genomic mechanisms. To this aim, the cardiovascular and the central nervous system provide excellent examples, where steroid hormones induce rapid vasodilatation and neuronal survival via non-genomic mechanisms, leading to relevant pathophysiological consequences. The evidence collected in the past Years indicates that target cells and organs are regulated by a complex interplay of genomic and non-genomic signaling mechanisms of steroid hormones, and the integrated action of these machineries has important functional roles in a variety of pathophysiological processes. The understanding of the molecular basis of the rapid effects of steroids is therefore important, and may in the future turn out to be of relevance for clinical purposes.
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Szczurowska, Ewa, Eszter Szánti-Pintér, Alena Randáková, Jan Jakubík, and Eva Kudova. "Allosteric Modulation of Muscarinic Receptors by Cholesterol, Neurosteroids and Neuroactive Steroids." International Journal of Molecular Sciences 23, no. 21 (October 28, 2022): 13075. http://dx.doi.org/10.3390/ijms232113075.
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Muscarinic acetylcholine receptors are membrane receptors involved in many physiological processes. Malfunction of muscarinic signaling is a cause of various internal diseases, as well as psychiatric and neurologic conditions. Cholesterol, neurosteroids, neuroactive steroids, and steroid hormones are molecules of steroid origin that, besides having well-known genomic effects, also modulate membrane proteins including muscarinic acetylcholine receptors. Here, we review current knowledge on the allosteric modulation of muscarinic receptors by these steroids. We give a perspective on the research on the non-genomic effects of steroidal compounds on muscarinic receptors and drug development, with an aim to ultimately exploit such knowledge.
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Chao, Helen M., Randall R. Sakai, Li Yun Ma, and Bruce S. McEwen. "Adrenal Steroid Regulation of Neurotrophic Factor Expression in the Rat Hippocampus." Endocrinology 139, no. 7 (July 1, 1998): 3112–18. http://dx.doi.org/10.1210/endo.139.7.6114.
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Abstract Adrenal steroids and neurotrophic factors are important modulators of neuronal plasticity, function, and survival in the rat hippocampus. Adrenal steroids act through two receptor subtypes, the glucocorticoid receptor (GR) and the mineralocorticoid receptor, and activation of each receptor subtype has distinct biochemical and physiological consequences. Adrenal steroids may exert their effects on neuronal structure and function through the regulation of expression of neurotrophic and growth-associated factors. We have examined adrenal steroid regulation of the neurotrophins brain-derived neurotrophic factor, neurotrophin-3, and basic fibroblast growth factor, as well as the growth associated protein GAP-43, through activation of GR or mineralocorticoid receptor with selective agonists. Our findings indicated that in CA2 pyramidal cells, adrenalectomy resulted in decreases in the levels of basic fibroblast growth factor and neurotrophin-3 messenger RNA, which were prevented by activation of mineralocorticoid but not glucocorticoid receptors. Adrenalectomy-induced increases in GAP-43 and brain-derived neurotrophic factor messenger RNA levels could be blocked by activation of glucocorticoid receptors in CA1, but not in CA3, pyramidal cells. Thus the extent to which adrenal steroids regulate hippocampal neurotrophic and growth-associated factors, appears to be dependent both on the adrenal steroid receptor subtype activated and on the hippocampal subregion examined.
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Mahfouz, Ahmed, Boudewijn P. F. Lelieveldt, Aldo Grefhorst, Lisa T. C. M. van Weert, Isabel M. Mol, Hetty C. M. Sips, José K. van den Heuvel, et al. "Genome-wide coexpression of steroid receptors in the mouse brain: Identifying signaling pathways and functionally coordinated regions." Proceedings of the National Academy of Sciences 113, no. 10 (January 25, 2016): 2738–43. http://dx.doi.org/10.1073/pnas.1520376113.
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Steroid receptors are pleiotropic transcription factors that coordinate adaptation to different physiological states. An important target organ is the brain, but even though their effects are well studied in specific regions, brain-wide steroid receptor targets and mediators remain largely unknown due to the complexity of the brain. Here, we tested the idea that novel aspects of steroid action can be identified through spatial correlation of steroid receptors with genome-wide mRNA expression across different regions in the mouse brain. First, we observed significant coexpression of six nuclear receptors (NRs) [androgen receptor (Ar), estrogen receptor alpha (Esr1), estrogen receptor beta (Esr2), glucocorticoid receptor (Gr), mineralocorticoid receptor (Mr), and progesterone receptor (Pgr)] with sets of steroid target genes that were identified in single brain regions. These coexpression relationships were also present in distinct other brain regions, suggestive of as yet unidentified coordinate regulation of brain regions by, for example, glucocorticoids and estrogens. Second, coexpression of a set of 62 known NR coregulators and the six steroid receptors in 12 nonoverlapping mouse brain regions revealed selective downstream pathways, such as Pak6 as a mediator for the effects of Ar and Gr on dopaminergic transmission. Third, Magel2 and Irs4 were identified and validated as strongly responsive targets to the estrogen diethylstilbestrol in the mouse hypothalamus. The brain- and genome-wide correlations of mRNA expression levels of six steroid receptors that we provide constitute a rich resource for further predictions and understanding of brain modulation by steroid hormones.
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Jones, Barbara B., and Martin Petkovich. "Targeting Transcription through Nuclear Receptors." Current Pharmaceutical Design 2, no. 1 (February 1996): 155–68. http://dx.doi.org/10.2174/1381612802666220920221247.
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Abstract: It has long been known that the structural modification of steroid hormones can alter their biological activity. Some of these changes in activity are attributable to altered uptake and metabolism. With the cDNA cloning and characterization of nuclear receptors for steroids and related compounds, it has become possible to ascribe changes in ligand activity to specific alterations in receptor function. In this review we will discuss the steroid/thyroid hormone receptor superfamily, and how knowledge of receptor structures and mechanism of action may be exploited therapeutically to alter their effects on gene expression in human disease states. We will discuss the basic structure of nuclear receptors and possible mechanisms by which their activities can be altered by ligands, both natural and synthetic. Later, we will focus on specific investigations related to the mechanism of action of some of the more widely studied antagonists. Finally we will examine the use of synthetic ligands and look at how determination of detailed receptor structures may help us to design more highly specific and effective ligands.
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Kadiyala, Vineela, and Catharine L. Smith. "Minireview: The Versatile Roles of Lysine Deacetylases in Steroid Receptor Signaling." Molecular Endocrinology 28, no. 5 (May 1, 2014): 607–21. http://dx.doi.org/10.1210/me.2014-1002.
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AbstractLysine deacetylases have been known to regulate nuclear receptor function for many years. In the unliganded state, nuclear receptors that form heterodimers with retinoid X receptors, such as the retinoic acid and thyroid hormone receptors, associate with deacetylases to repress target genes. In the case of steroid receptors, binding of an antagonist ligand was initially reported to induce association of deacetylases to prevent activation of target genes. Since then, deacetylases have been shown to have diverse functions in steroid receptor signaling, from regulating interactions with molecular chaperones to facilitating their ability to activate transcription. The purpose of this review is to summarize recent studies on the role of deacetylases in steroid receptor signaling, which show deacetylases to be highly versatile regulators of steroid receptor function.
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WEIGEL, Nancy L. "Steroid hormone receptors and their regulation by phosphorylation." Biochemical Journal 319, no. 3 (November 1, 1996): 657–67. http://dx.doi.org/10.1042/bj3190657.
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The steroid/thyroid hormone receptor superfamily of ligand-activated transcription factors encompasses not only the receptors for steroids, thyroid hormone, retinoids and vitamin D, but also a large number of proteins whose functions and/or ligands are unknown and which are thus termed orphan receptors. Recent studies have highlighted the importance of phosphorylation in receptor function. Although most of the phosphorylation sites are serine and threonine residues, a few of the family members are also phosphorylated on tyrosine. Those steroid receptor family members that are bound to heat-shock proteins in the absence of ligand typically are basally phosphorylated and exhibit increases in phosphorylation upon ligand binding. Most of these sites contain Ser-Pro motifs, and there is evidence that cyclin-dependent kinases and MAP kinases (mitogen-activated protein kinases) phosphorylate subsets of these sites. In contrast, phosphorylation sites identified thus far in members of the family that bind to DNA in the absence of hormone typically do not contain Ser-Pro motifs and are frequently casein kinase II or protein kinase A sites. Phosphorylation has been implicated in DNA binding, transcriptional activation and stability of the receptors. The finding that some of the steroid receptor family members can be activated in the absence of ligand by growth factors or neurotransmitters that modulate kinase and/or phosphatase pathways underscores the role of phosphorylation in receptor function. Hence this family of transcription factors integrates signals from ligands as well as from signal transduction pathways, resulting in alterations in mRNA and protein expression that are unique to the complex signals received.
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Evaul, Kristen, Michelle Jamnongjit, Bala Bhagavath, and Stephen R. Hammes. "Testosterone and Progesterone Rapidly Attenuate Plasma Membrane Gβγ-Mediated Signaling in Xenopus laevis Oocytes by Signaling through Classical Steroid Receptors." Molecular Endocrinology 21, no. 1 (January 1, 2007): 186–96. http://dx.doi.org/10.1210/me.2006-0301.
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Abstract Many transcription-independent (nongenomic) steroid effects are regulated by G proteins. A well-established, biologically relevant example of steroid/G protein interplay is steroid-triggered oocyte maturation, or meiotic resumption, in Xenopus laevis. Oocyte maturation is proposed to occur through a release of inhibition mechanism whereby constitutive signaling by Gβγ and other G proteins maintains oocytes in meiotic arrest. Steroids (androgens in vivo, and androgens and progesterone in vitro) overcome this inhibition to promote meiotic resumption. To test this model, we used G protein-regulated inward rectifying potassium channels (GIRKs) as markers of Gβγ activity. Overexpression of GIRKs 1 and 2 in Xenopus oocytes resulted in constitutive potassium influx, corroborating the presence of basal Gβγ signaling in resting oocytes. Testosterone and progesterone rapidly reduced potassium influx, validating that steroids attenuate Gβγ activity. Interestingly, reduction of classical androgen receptor (AR) expression by RNA interference abrogated testosterone’s effects on GIRK activity at low, but not high, steroid concentrations. Accordingly, androgens bound to the Xenopus progesterone receptor (PR) at high concentrations, suggesting that, in addition to the AR, the PR might mediate G protein signaling when androgens levels are elevated. In contrast, progesterone bound with high affinity to both the Xenopus PR and AR, indicating that progesterone might signal and promote maturation through both receptors, regardless of its concentration. In sum, these studies introduce a novel method for detecting nongenomic steroid effects on G proteins in live cells in real time, and demonstrate that cross talk may occur between steroids and their receptors during Xenopus oocyte maturation.
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Kahn, SM, DJ Hryb, AM Nakhla, NA Romas, and W. Rosner. "Sex hormone-binding globulin is synthesized in target cells." Journal of Endocrinology 175, no. 1 (October 1, 2002): 113–20. http://dx.doi.org/10.1677/joe.0.1750113.
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Sex hormone-binding globulin (SHBG) is a multifunctional protein that acts in humans to regulate the response to steroids at several junctures. It was originally described as a hepatically secreted protein that is the major binding protein for sex steroids in plasma, thereby regulating the availability of free steroids to hormone-responsive tissues. SHBG also functions as part of a novel steroid-signaling system that is independent of the classical intracellular steroid receptors. Unlike the intracellular steroid receptors that are ligand-activated transcription factors, SHBG mediates androgen and estrogen signaling at the cell membrane by way of cAMP. We have reviewed the current state of knowledge on the SHBG gene and the role of SHBG in steroid signaling (we shall not address its function as a plasma-binding protein).
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Bishop, J. Michael. "Steroid receptors: Oncogenes as hormone receptors." Nature 321, no. 6066 (May 1986): 112–13. http://dx.doi.org/10.1038/321112a0.
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Ruka, Kristen A., Laura L. Burger, and Suzanne M. Moenter. "Both Estrogen and Androgen Modify the Response to Activation of Neurokinin-3 and κ-Opioid Receptors in Arcuate Kisspeptin Neurons From Male Mice." Endocrinology 157, no. 2 (November 12, 2015): 752–63. http://dx.doi.org/10.1210/en.2015-1688.
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Abstract Gonadal steroids regulate the pattern of GnRH secretion. Arcuate kisspeptin (kisspeptin, neurokinin B, and dynorphin [KNDy]) neurons may convey steroid feedback to GnRH neurons. KNDy neurons increase action potential firing upon the activation of neurokinin B receptors (neurokinin-3 receptor [NK3R]) and decrease firing upon the activation of dynorphin receptors (κ-opioid receptor [KOR]). In KNDy neurons from intact vs castrated male mice, NK3R-mediated stimulation is attenuated and KOR-mediated inhibition enhanced, suggesting gonadal secretions are involved. Estradiol suppresses spontaneous GnRH neuron firing in male mice, but the mediators of the effects on firing in KNDy neurons are unknown. We hypothesized the same gonadal steroids affecting GnRH firing pattern would regulate KNDy neuron response to NK3R and KOR agonists. To test this possibility, extracellular recordings were made from KNDy neurons in brain slices from intact, untreated castrated or castrated adult male mice treated in vivo with steroid receptor agonists. As observed previously, the stimulation of KNDy neurons by the NK3R agonist senktide was attenuated in intact vs castrated mice and suppression by dynorphin was enhanced. In contrast to observations of steroid effects on the GnRH neuron firing pattern, both estradiol and DHT suppressed senktide-induced KNDy neuron firing and enhanced the inhibition caused by dynorphin. An estrogen receptor-α agonist but not an estrogen receptor-β agonist mimicked the effects of estradiol on NK3R activation. These observations suggest the steroid modulation of responses to activation of NK3R and KOR as mechanisms for negative feedback in KNDy neurons and support the contribution of these neurons to steroid-sensitive elements of a GnRH pulse generator.
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Chow, Renee W. Y., David J. Handelsman, and Martin K. C. Ng. "Minireview: Rapid Actions of Sex Steroids in the Endothelium." Endocrinology 151, no. 6 (April 14, 2010): 2411–22. http://dx.doi.org/10.1210/en.2009-1456.
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The endothelium is a dynamic interface between the blood vessel and the circulating blood that plays a pivotal role in vascular homeostasis. As such, studies on sex steroid regulation of endothelial function are critical to understanding the role of sex steroids in cardiovascular health and disease. The classical model of steroid action involves liganded steroid receptors binding to specific response elements on target genes to regulate gene transcription. In whole organisms, the time lag between steroid administration and observable effects produced by newly synthesized protein is typically in the order of hours to days. And yet, some effects of steroids, such as vasodilatation, occur within seconds to minutes of steroid administration. Studies in multiple cell types have also shown that steroids can cause the rapid initiation of multiple signaling cascades and second messenger systems, prompting investigations into alternate, transcription independent mechanisms of steroid action. Studies of the endothelium over the past two decades have revealed fundamental mechanisms in rapid sex steroid signaling. In particular, endothelium-dependent vasodilatation by estradiol-induced activation of endothelial nitric oxide synthase has proven to be an uniquely informative model to study sex steroid signaling via classical sex steroid receptors localized to the cell membrane. Despite the complexity of feedback and cross talk between rapid sex steroid signaling and other modes of steroid action, recent studies in this field are facilitating the development of steroidal drugs that selectively target the ability of sex steroids to initiate signaling cascades.
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Stephenson, G., and J. Funder. "Hippocampal and renal type I receptors are differentially regulated." American Journal of Physiology-Endocrinology and Metabolism 252, no. 4 (April 1, 1987): E525—E529. http://dx.doi.org/10.1152/ajpendo.1987.252.4.e525.
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Previously, we have shown that renal mineralocorticoid receptors and hippocampal "corticosterone-perferring" sites have identical intrinsic steroid specificity in vitro. Others have shown that the aldosterone binding species in kidney and hippocampus have identical trypsin fragmentation patterns on isoelectric focusing. To further explore possible areas of identity, we determined levels of type I receptors in hippocampus, renal outer medulla cortex, and renal inner medulla papilla from 22 min to 16 days after adrenalectomy. Available type I sites in kidney fractions increased postadrenalectomy to plateau levels in 22 (inner medulla papilla) or 90 min (outer medulla cortex). In contrast, available hippocampal receptors attained maximal levels 24-48 h postadrenalectomy. Animals, 24-h adrenalectomized, showed no differences in steroid uptake or washout between kidney and hippocampus, determined by in vitro tracer binding 22 or 90 min after intravenous aldosterone or corticosterone. We interpret the marked difference in receptor levels between kidney and hippocampus postadrenalectomy as evidence for tissue-specific differences in the control of receptor levels by endogenous steroids.
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Tejura, S., G. R. Rodgers, M. H. Dunion, M. A. Parsons, J. C. E. Underwood, and P. M. Ingleton. "Sex-steroid receptors in the diethylnitrosamine model of hepatocarcinogenesis: modifications by gonadal ablation and steroid replacement therapy." Journal of Molecular Endocrinology 3, no. 3 (November 1989): 229–37. http://dx.doi.org/10.1677/jme.0.0030229.
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ABSTRACT The results of this study confirm our previous report of increased androgen receptor expression in livers of female SUAH Wistar rats during development of liver tumours induced by diethylnitrosamine (DENA). In adult female rats not treated with DENA, removal of the ovary increased liver androgen receptor levels but testosterone did not further enhance the androgen receptor status of ovariectomized rats. In normal adult males the testis and/or testosterone maintained high levels of androgen receptors but oestrogen reduced them in castrated rats. Oestrogen receptor levels were not significantly changed in either males or females by gonadectomy. Treatment of female rats with DENA for 10 and 16 weeks increased liver androgen receptors but oestrogen receptors were only reduced by 16 weeks of DENA treatment, whether the rats were intact or ovariectomized. Concentrations of liver androgen receptors were increased in intact and castrated male rats by 10 and 16 weeks of DENA treatment, an increase not seen in the previous experiments. Oestrogen appeared to inhibit both the increases in liver androgen receptor expression and liver tumour development in rats treated with the weakly carcinogenic dose of 10 weeks of DENA. However, the full carcinogenic dose of 16 weeks of DENA increased liver androgen receptors and decreased oestrogen receptors in female rats regardless of sex-steroid status. Development of malignant hepatocellular carcinoma (HCC) was associated with both an increase in liver androgen receptors and a decrease in oestrogen receptors. Maintenance of relatively high levels of liver oestrogen receptors appeared to protect the liver against development of HCC.
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Das, Shampa, and Peter Thomas. "Pesticides Interfere with the Nongenomic Action of a Progestogen on Meiotic Maturation by Binding to its Plasma Membrane Receptor on Fish Oocytes." Endocrinology 140, no. 4 (April 1, 1999): 1953–56. http://dx.doi.org/10.1210/endo.140.4.6781.
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Abstract Although many environmental contaminants disrupt endocrine function by binding to nuclear steroid receptors, it is not known whether they are capable of binding to steroid membrane receptors and interfering with nongenomic actions of steroids. The binding of several organochlorine pesticides to the plasma membrane receptor for the maturation-inducing steroid, 17,20β,21-trihydroxy-4-pregnen-3-one (20β-S), in the ovaries of spotted seatrout (Cynoscion nebulosus) was investigated in in vitro competition assays. Kepone and o,p′-DDD were competitive inhibitors of 20β-S binding and caused concentration-dependent displacement of [3H]-20β-S from its receptor site over the range of 10−4 to 10−6 or 10−7 M, whereas several other pesticides had lower affinities for the receptor. Interference with the nongenomic actions of 20β-S on final meiotic maturation of spotted seatrout oocytes (final oocyte maturation, FOM) was examined in an in vitro bioassay. A concentration-dependent inhibition of FOM in response to 20β-S was observed after 5 min and 12 h exposure to the same range of Kepone and o,p′-DDD concentrations (10−4 to 10−6 or 10−7 M). The close correspondence between competitive binding of the two pesticides to the 20β-S membrane receptor and their inhibition of 20β-S induced FOM suggests a mechanism of endocrine disruption mediated by binding to a steroid membrane receptor and antagonism of a nongenomic steroid action.
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Meikle, A., C. Tasende, C. Sosa, and E. G. Garófalo. "The role of sex steroid receptors in sheep female reproductive physiology." Reproduction, Fertility and Development 16, no. 4 (2004): 385. http://dx.doi.org/10.1071/rd04036.
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Cell responsiveness to steroid hormones is related to the number and affinity of its receptors, thus factors affecting steroid expression will influence tissue sensitivity and functionality. The present review discusses the role of oestrogen and progesterone receptors in sheep female reproductive physiology. The mechanism of steroid hormone action in the target cell is introduced first; the tissue distribution, physiological functions and regulation of oestrogen receptor subtypes and progesterone receptor isoforms in ruminants are reported. The role of steroid receptors in target tissues (with emphasis on the uterus and pituitary gland) during different physiological events is addressed in an attempt to clarify oestrogen and progesterone actions in different developmental and reproductive stages: prepubertal period, oestrous cycle, pregnancy, post-partum period and seasonal anoestrus. The present review shows how the distinct reproductive stages are accompanied by dramatic changes in uterine receptor expression. The role of oestrogen and progesterone receptors in the molecular mechanism responsible for premature luteolysis that results in subnormal luteal function is discussed. Finally, the effect of nutrition on sex steroid receptor expression and the involvement on reproductive performance is reported.
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Picard, D. "Molecular mechanisms of cross-talk between growth factors and nuclear receptor signaling." Pure and Applied Chemistry 75, no. 11-12 (January 1, 2003): 1743–56. http://dx.doi.org/10.1351/pac200375111743.
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Signaling pathways can be linear, but more complex patterns are common. Growth factors and many other extracellular signals cannot directly enter cells and transduce their information via membrane-bound receptors. In contrast, steroid receptors are members of the nuclear receptor superfamily and await their cognate hormones inside the cells. These two types of signaling pathways are extensively intertwined and crosstalk at many different levels. A wide range of extra- and intracellular signals, including a variety of growth factors, can activate the transcriptional activity of steroid receptors in the absence of their cognate hormones. Conversely, steroid receptors lead a double life. By coupling to signaling molecules that mediate signal transduction of extracellular factors, they can elicit very rapid nongenomic responses. The signaling pathways of steroid-independent activation of steroid receptors, on the one hand, and of nongenomic signaling by steroid receptors, on the other, display a remarkable reciprocal relationship suggesting that these two modes of signaling crosstalk may be two faces of the same coin.
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Ide, Hiroki, and Hiroshi Miyamoto. "Steroid Hormone Receptor Signals as Prognosticators for Urothelial Tumor." Disease Markers 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/840640.
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There is a substantial amount of preclinical or clinical evidence suggesting that steroid hormone receptor-mediated signals play a critical role in urothelial tumorigenesis and tumor progression. These receptors include androgen receptor, estrogen receptors, glucocorticoid receptor, progesterone receptor, vitamin D receptor, retinoid receptors, peroxisome proliferator-activated receptors, and others including orphan receptors. In particular, studies using urothelial cancer tissue specimens have demonstrated that elevated or reduced expression of these receptors as well as alterations of their upstream or downstream pathways correlates with patient outcomes. This review summarizes and discusses available data suggesting that steroid hormone receptors and related signals serve as biomarkers for urothelial carcinoma and are able to predict tumor recurrence or progression.
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Parker, Malcolm G. "Steroid and related receptors." Current Opinion in Cell Biology 5, no. 3 (June 1993): 499–504. http://dx.doi.org/10.1016/0955-0674(93)90016-j.
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Auricchio, Ferdinando. "Phosphorylation of steroid receptors." Journal of Steroid Biochemistry 32, no. 4 (April 1989): 613–22. http://dx.doi.org/10.1016/0022-4731(89)90397-x.
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Fuller, Peter J. "Steroid receptors as oncogenes?" Molecular and Cellular Endocrinology 59, no. 3 (October 1988): 161–64. http://dx.doi.org/10.1016/0303-7207(88)90099-8.
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Marugo, Mario, G. Torre, D. Bernasconi, L. Fazzuoli, S. Berta, and G. Giordano. "Thyroid and steroid receptors." Journal of Endocrinological Investigation 12, no. 8 (September 1989): 565–70. http://dx.doi.org/10.1007/bf03350762.
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Dougherty, John J., Raj K. Puri, and David O. Toft. "Phosphorylation of steroid receptors." Trends in Pharmacological Sciences 6 (January 1985): 83–85. http://dx.doi.org/10.1016/0165-6147(85)90034-3.
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Challa, Venkata R. "Steroid receptors in meningiomas." Surgical Neurology 28, no. 3 (September 1987): 232. http://dx.doi.org/10.1016/0090-3019(87)90142-x.
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Cato, Laura, Antje Neeb, Myles Brown, and Andrew C. B. Cato. "Control of Steroid Receptor Dynamics and Function by Genomic Actions of the Cochaperones p23 and Bag-1L." Nuclear Receptor Signaling 12, no. 1 (January 2014): nrs.12005. http://dx.doi.org/10.1621/nrs.12005.
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Molecular chaperones encompass a group of unrelated proteins that facilitate the correct assembly and disassembly of other macromolecular structures of which they themselves do not remain a part. Chaperones associate with a large and diverse set of cofactors termed cochaperones that regulate their function and specificity. Chaperones and cochaperones regulate the activity of several classes of signaling molecules, including steroid receptors. Upon binding ligand, steroid receptors interact with discrete nucleotide sequences within the nucleus to control the expression of diverse physiological and developmental genes. Molecular chaperones and cochaperones are typically known to provide the correct conformation for ligand binding by the steroid receptors. While this contribution is widely accepted, recent studies have reported that they further modulate steroid receptor action outside ligand binding. Specifically, they are thought to contribute to receptor turnover, transport of the receptor to different subcellular localizations, recycling of the receptor on chromatin and stabilization of receptor DNA binding. In addition to these combined effects with molecular chaperones, cochaperones have additional functions that are independent of molecular chaperones, some of which impact steroid receptor action. Two well-studied examples are the cochaperones p23 and Bag-1L, which have been identified as modulators of steroid receptor activity in the nucleus. Understanding details of their regulatory action will provide new therapeutic opportunities for controlling steroid receptor action independent of the widespread effects of molecular chaperones.
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Weigel, Nancy L., and Nicole L. Moore. "Kinases and protein phosphorylation as regulators of steroid hormone action." Nuclear Receptor Signaling 5, no. 1 (January 2007): nrs.05005. http://dx.doi.org/10.1621/nrs.05005.
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Although the primary signal for the activation of steroid hormone receptors is binding of hormone, there is increasing evidence that the activities of cell signaling pathways and the phosphorylation status of these transcription factors and their coregulators determine the overall response to the hormone. In some cases, enhanced cell signaling is sufficient to cause activation of receptors in medium depleted of steroids. Steroid receptors are targets for multiple kinases. Many of the phosphorylation sites contain Ser/Thr-Pro motifs implicating proline-directed kinases such as the cyclin-dependent kinases and the mitogen-activated kinases (MAPK) in receptor phosphorylation. Although some sites are constitutively phosphorylated, others are phosphorylated in response to hormone. Still others are only phosphorylated in response to specific cell signaling pathways. Phosphorylation of specific sites has been implicated not only in overall transcriptional activity, but also in nuclear localization, protein stability, and DNA binding. The studies of the roles of phosphorylation in coregulator function are more limited, but it is now well established that many of them are highly phosphorylated and that phosphorylation regulates their function. There is good evidence that some of the phosphorylation sites in the receptors and coregulators are targets of multiple signaling pathways. Individual sites have been associated both with functions that enhance the activity of the receptor, as well as with functions that inhibit activity. Thus, the specific combinations of phosphorylations of the steroid receptor combined with the expression levels and phosphorylation status of coregulators will determine the genes regulated and the biological response.
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Levin, Ellis R. "Rapid signaling by steroid receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 5 (November 2008): R1425—R1430. http://dx.doi.org/10.1152/ajpregu.90605.2008.
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Steroid receptors transcribe genes that lead to important biological processes, including normal organ development and function, tissue differentiation, and promotion of oncogenic transformation. These actions mainly result from nuclear steroid receptor action. However, for 50 years, it has been known that rapid effects of steroid hormones occur and could result from rapid signal transduction. Examples of these effects include stress responses to secreted glucocorticoids, rapid actions of thyroid hormones in the heart, and acute uterine/vaginal responses to injected estrogen. These types of responses have increasingly been attributed to rapid signaling by steroid hormones, upon engaging binding proteins most often at the cell surface of target organs. It is clear that rapid signal transduction serves an integrated role to modify existing proteins, altering their structure and activity, and to modulate gene transcription, often through collaboration with the nuclear pool of steroid receptors. The biological outcomes of steroid hormone actions thus reflect input from various cellular pools, cocoordinating the necessary events that are restrained in temporal and kinetic fashion. Here I describe the current understanding of rapid steroid signaling that is now appreciated to extend to virtually all members of this family of hormones and their receptors.
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Wendler, Alexandra, Elisabetta Baldi, Brian J. Harvey, Angel Nadal, Anthony Norman, and Martin Wehling. "Position Paper: Rapid responses to steroids: current status and future prospects." European Journal of Endocrinology 162, no. 5 (May 2010): 825–30. http://dx.doi.org/10.1530/eje-09-1072.
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Steroids exert their actions through several pathways. The classical genomic pathway, which involves binding of steroids to receptors and subsequent modulation of gene expression, is well characterized. Besides this, rapid actions of steroids have been shown to exist. Since 30 years, research on rapid actions of steroids is an emerging field of science. Today, rapid effects of steroids are well established, and are shown to exist for every type of steroid. The classical steroid receptors have been shown to be involved in rapid actions, but there is also strong evidence that unrelated structures mediate these rapid effects. Despite increasing knowledge about the mechanisms and structures which mediate these actions, there is still no unanimous acceptance of this category. This article briefly reviews the history of the field including current controversies and challenges. It is not meant as a broad review of literature, but should increase the awareness of the endocrinology society for rapid responses to steroids. As members of the organizing committee of the VI International Meeting on Rapid Responses to Steroid Hormones 2009, we propose a research agenda focusing on the identification of new receptoral structures and the identification of mechanisms of actions at physiological steroid concentrations. Additionally, efforts for the propagation of translational studies, which should finally lead to clinical benefit in the area of rapid steroid action research, should be intensified.
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Szczurowska, Ewa, Eszter Szánti-Pintér, Nikolai Chetverikov, Alena Randáková, Eva Kudová, and Jan Jakubík. "Modulation of Muscarinic Signalling in the Central Nervous System by Steroid Hormones and Neurosteroids." International Journal of Molecular Sciences 24, no. 1 (December 28, 2022): 507. http://dx.doi.org/10.3390/ijms24010507.
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Muscarinic acetylcholine receptors expressed in the central nervous system mediate various functions, including cognition, memory, or reward. Therefore, muscarinic receptors represent potential pharmacological targets for various diseases and conditions, such as Alzheimer’s disease, schizophrenia, addiction, epilepsy, or depression. Muscarinic receptors are allosterically modulated by neurosteroids and steroid hormones at physiologically relevant concentrations. In this review, we focus on the modulation of muscarinic receptors by neurosteroids and steroid hormones in the context of diseases and disorders of the central nervous system. Further, we propose the potential use of neuroactive steroids in the development of pharmacotherapeutics for these diseases and conditions.
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Clairardin, Sandrine G., Ryan T. Paitz, and Rachel M. Bowden. "In ovo inhibition of steroid metabolism by bisphenol-A as a potential mechanism of endocrine disruption." Proceedings of the Royal Society B: Biological Sciences 280, no. 1769 (October 22, 2013): 20131773. http://dx.doi.org/10.1098/rspb.2013.1773.
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During embryonic development, endogenous signals, for example steroid hormones, and exogenous signals, for example endocrine disrupting chemicals (EDCs), have the capacity to produce phenotypic effects that persist into adulthood. As the actions of steroids are mediated through the binding of steroid receptors, most studies of EDCs have assumed that they too elicit their effects by binding steroid receptors. We tested an alternative hypothesis, namely that EDCs elicit their effects during embryonic development by disrupting the metabolism of maternally derived steroids, thereby allowing maternally derived steroids to bind steroid receptors and elicit effects. Specifically, we examined the ability of the EDC, bisphenol-A (BPA) to inhibit the normal metabolism of oestradiol during the first nine days of embryonic development in the red-eared slider turtle ( Trachemys scripta ). We found that, when BPA was present, oestrogen metabolism was inhibited when compared to control eggs. In particular, the formation of oestrone sulfate was blocked in BPA-treated eggs. We postulate that the oestrogenic effects of EDCs may be driven, at least in part, by inappropriate oestrogen signalling. The retention of oestrogens at points of development when they would normally be metabolized to inactive forms might also help explain low-dose effects frequently reported for EDCs.
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Sheppard, Karen E. "II. Intestinal corticosteroid receptors." American Journal of Physiology-Gastrointestinal and Liver Physiology 282, no. 5 (May 1, 2002): G742—G746. http://dx.doi.org/10.1152/ajpgi.00531.2001.
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Two corticosteroid receptors have been cloned; they are the glucocorticoid receptor and the mineralocorticoid receptor. These receptors are members of the steroid/thyroid/retinoid receptor family of nuclear transactivating factors, which are characterized by two highly conserved zinc fingers in the central DNA binding domain, a COOH-terminal domain that encompasses the ligand binding site, and a variable NH2-terminal domain. In addition to these cloned receptors, other corticosteroid receptors have recently been identified in intestine. Steroid binding studies have identified two novel putative corticosteroid receptors in intestinal epithelia, and molecular cloning studies have detected two low-affinity receptors in small intestine that are activated by corticosteroids and induce CYP3A gene expression. This article focuses on the identification of these novel corticosteroid receptors and the potential role they may play in intestinal physiology.
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Keigley, Quinton J., Amy M. Fowler, Sophia R. O'Brien, and Farrokh Dehdashti. "Molecular Imaging of Steroid Receptors in Breast Cancer." Cancer Journal 30, no. 3 (May 2024): 142–52. http://dx.doi.org/10.1097/ppo.0000000000000715.
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Abstract Steroid receptors regulate gene expression for many important physiologic functions and pathologic processes. Receptors for estrogen, progesterone, and androgen have been extensively studied in breast cancer, and their expression provides prognostic information as well as targets for therapy. Noninvasive imaging utilizing positron emission tomography and radiolabeled ligands targeting these receptors can provide valuable insight into predicting treatment efficacy, staging whole-body disease burden, and identifying heterogeneity in receptor expression across different metastatic sites. This review provides an overview of steroid receptor imaging with a focus on breast cancer and radioligands for estrogen, progesterone, and androgen receptors.
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Sánchez, Edwin R. "Steroid hormone receptors: Basic and clinical aspects—Proceedings meadowbrook conference on steroid receptors." Trends in Endocrinology & Metabolism 5, no. 5 (July 1994): 223–25. http://dx.doi.org/10.1016/1043-2760(94)90086-8.
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Ma, Zhi-Qing, Zheng Liu, Elly S. W. Ngan, and Sophia Y. Tsai. "Cdc25B Functions as a Novel Coactivator for the Steroid Receptors." Molecular and Cellular Biology 21, no. 23 (December 1, 2001): 8056–67. http://dx.doi.org/10.1128/mcb.21.23.8056-8067.2001.
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ABSTRACT We have previously demonstrated that overexpression of Cdc25B in transgenic mice resulted in mammary gland hyperplasia and increased steroid hormone responsiveness. To address how Cdc25B enhances the hormone responsiveness in mammary glands, we showed that Cdc25B stimulates steroid receptor-dependent transcription in transient transfection assays and in a cell-free assay with chromatin templates. Surprisingly, the effect of Cdc25B on steroid receptors is independent of its protein phosphatase activity in vitro. The direct interactions of Cdc25B with steroid receptors, on the other hand, were evidenced in in vivo and in vitro assays, suggesting the potential direct contribution of Cdc25B on the steroid receptor-mediated transcription. In addition, p300/CBP-associated factor and CREB binding protein were shown to interact and synergize with Cdc25B and further enhance its coactivation activity. Thus, we have uncovered a novel function of Cdc25B that serves as a steroid receptor coactivator in addition to its role as a regulator for cell cycle progression. This dual function might likely contribute to its oncogenic action in breast cancer.
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Branković-Magić, M., Z. Nešković-Konstantinović, D. Nikolić-Vukosavljević, and I. Spužić. "Steroid receptors in pleural effusions of advanced breast cancer patients." International Journal of Biological Markers 10, no. 3 (July 1995): 143–48. http://dx.doi.org/10.1177/172460089501000303.
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The steroid receptor content in breast carcinoma correlates with the responsiveness of malignant cells to endocrine manipulation. Although the steroid receptor status of the primary tumor is mostly used to select systemic therapy, it was suggested that steroid receptor content should be evaluated in metastatic lesions whenever possible. In this study the estrogen and progesterone receptor content was determined biochemically in 38 pleural effusions from advanced breast cancer patients. In 17/38 patients the steroid receptor status was assessed twice during the course of the disease - at diagnosis in the primary tumor/lymph nodes, and subsequently in metastatic pleural effusion fluid. A trend towards lower receptor values in pleural fluids was evident. There was no correlation between pleural steroid receptor content and pleural response to endocrine or chemo/endocrine therapy, indicating that the usefulness of effusional steroid receptors for therapy planning of advanced breast cancer could not be confirmed in this study.
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Zheng, Yingfeng, and Leigh C. Murphy. "Regulation of Steroid Hormone Receptors and Coregulators during the Cell Cycle Highlights Potential Novel Function in Addition to Roles as Transcription Factors." Nuclear Receptor Signaling 14, no. 1 (January 2016): nrs.14001. http://dx.doi.org/10.1621/nrs.14001.
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Cell cycle progression is tightly controlled by several kinase families including Cyclin-Dependent Kinases, Polo-Like Kinases, and Aurora Kinases. A large amount of data show that steroid hormone receptors and various components of the cell cycle, including cell cycle regulated kinases, interact, and this often results in altered transcriptional activity of the receptor. Furthermore, steroid hormones, through their receptors, can also regulate the transcriptional expression of genes that are required for cell cycle regulation. However, emerging data suggest that steroid hormone receptors may have roles in cell cycle progression independent of their transcriptional activity. The following is a review of how steroid receptors and their coregulators can regulate or be regulated by the cell cycle machinery, with a particular focus on roles independent of transcription in G2/M.
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Savory, Joanne G. A., Gratien G. Préfontaine, Claudia Lamprecht, Mingmin Liao, Rhian F. Walther, Yvonne A. Lefebvre, and Robert J. G. Haché. "Glucocorticoid Receptor Homodimers and Glucocorticoid-Mineralocorticoid Receptor Heterodimers Form in the Cytoplasm through Alternative Dimerization Interfaces." Molecular and Cellular Biology 21, no. 3 (February 1, 2001): 781–93. http://dx.doi.org/10.1128/mcb.21.3.781-793.2001.
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ABSTRACT Steroid hormone receptors act to regulate specific gene transcription primarily as steroid-specific dimers bound to palindromic DNA response elements. DNA-dependent dimerization contacts mediated between the receptor DNA binding domains stabilize DNA binding. Additionally, some steroid receptors dimerize prior to their arrival on DNA through interactions mediated through the receptor ligand binding domain. In this report, we describe the steroid-induced homomeric interaction of the rat glucocorticoid receptor (GR) in solution in vivo. Our results demonstrate that GR interacts in solution at least as a dimer, and we have delimited this interaction to a novel interface within the hinge region of GR that appears to be both necessary and sufficient for direct binding. Strikingly, we also demonstrate an interaction between GR and the mineralocorticoid receptor in solution in vivo that is dependent on the ligand binding domain of GR alone and is separable from homodimerization of the glucocorticoid receptor. These results indicate that functional interactions between the glucocorticoid and mineralocorticoid receptors in activating specific gene transcription are probably more complex than has been previously appreciated.
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Fliss, Albert E., Yifang Fang, Frank Boschelli, and Avrom J. Caplan. "Differential In Vivo Regulation of Steroid Hormone Receptor Activation by Cdc37p." Molecular Biology of the Cell 8, no. 12 (December 1997): 2501–9. http://dx.doi.org/10.1091/mbc.8.12.2501.
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The CDC37 gene is essential for the activity of p60v-src when expressed in yeast cells. Since the activation pathway for p60v-src and steroid hormone receptors is similar, the present study analyzed the hormone-dependent transactivation by androgen receptors and glucocorticoid receptors in yeast cells expressing a mutant version of the CDC37gene. In this mutant, hormone-dependent transactivation by androgen receptors was defective at both permissive and restrictive temperatures, although transactivation by glucocorticoid receptors was mildly defective only at the restrictive temperature. Cdc37p appears to function via the androgen receptor ligand-binding domain, although it does not influence receptor hormone-binding affinity. Models for Cdc37p regulation of steroid hormone receptors are discussed.
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Fannon, Stacey A., Regina M. Vidaver, and Sherry A. Marts. "Historical Perspectives: An abridged history of sex steroid hormone receptor action." Journal of Applied Physiology 91, no. 4 (October 1, 2001): 1854–59. http://dx.doi.org/10.1152/jappl.2001.91.4.1854.
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The field of steroid hormone action is well established, although it is barely more than four decades old. Pivotal experiments in the late 1950s and 1960s showed that hormone-binding components exist within nuclei of target tissues and that steroid hormones act by regulating gene expression, rather than directly influencing enzymatic processes. The understanding that steroid hormone receptors interact with the general transcription machinery and alter chromatin structure came in the 1970s and 1980s, and details of this mechanism continue to be elucidated. In addition, the discovery of rapid cellular responses to steroid hormones has led to the identification of putative membrane-bound steroid receptors that act without affecting gene transcription. As noted in the recent Institute of Medicine report Exploring the Biological Contributions to Human Health: Does Sex Matter?, the effects of steroid hormones and defects in steroid hormone receptor action have a profound impact on human health and disease. Future research directives include the development of potent, selective steroid receptor modulators, the elucidation of nongenomic steroid hormone effects, and further exploration of hormone-genome interactions.