Journal ArticleDOI
Mineralocorticoid and glucocorticoid receptor activities distinguished by nonreceptor factors at a composite response element
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TLDR
The distinct physiologic effects mediated by MR and GR may be determined by differential interactions of nonreceptor factors with specific receptor domains at composite response elements at plfG, a 25-base pair composite response element to which both the steroid receptors and transcription factor AP1 can bind.Abstract:
Mineralocorticoid and glucocorticoid hormones elicit distinct physiologic responses, yet the mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) bind to and activate transcription similarly from a consensus simple hormone response element (HRE). The activities of GR and MR at plfG, a 25-base pair composite response element to which both the steroid receptors and transcription factor AP1 can bind, are analyzed here. Under conditions in which GR represses AP1-stimulated transcription from plfG, MR was inactive. With the use of MR-GR chimeras, a segment of the NH2-terminal region of GR (amino acids 105 to 440) was shown to be required for this repression. Thus, the distinct physiologic effects mediated by MR and GR may be determined by differential interactions of nonreceptor factors with specific receptor domains at composite response elements.read more
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Journal ArticleDOI
How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions.
TL;DR: This review considers recent findings regarding GC action and generates criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stress-response or, as an additional category, is preparative for a subsequent stressor.
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Brain corticosteroid receptor balance in health and disease.
TL;DR: The balance in actions mediated by the two corticosteroid receptor types in these neurons appears critical for neuronal excitability, stress responsiveness, and behavioral adaptation and Dysregulation of this MR/GR balance brings neurons in a vulnerable state with consequences for regulation of the stress response and enhanced vulnerability to disease in genetically predisposed individuals.
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Limbic system mechanisms of stress regulation: hypothalamo-pituitary-adrenocortical axis.
TL;DR: The influence of the limbic system on the HPA axis is likely the end result of the overall patterning of responses to given stimuli and glucocorticoids, with the magnitude of the secretory response determined with respect to the relative contributions of the various structures.
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The anti-inflammatory and immunosuppressive effects of glucocorticoids, recent developments and mechanistic insights
TL;DR: A greater understanding is required of the mechanisms by which glucocorticoids exert their anti-inflammatory and immunosuppressive actions, and recent research is shedding new light on some of these mechanisms and has produced some surprising new findings.
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The length and location of CAG trinucleotide repeats in the androgen receptor N-terminal domain affect transactivation function
TL;DR: It is postulate that this residual AR activity may be sufficient for development of male primary and secondary sex characteristics, but may fall below a threshold level of activity necessary for normal maintenance of motor neuron function.
References
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Journal ArticleDOI
Cloning of human mineralocorticoid receptor complementary DNA: structural and functional kinship with the glucocorticoid receptor
Jeffrey L. Arriza,Jeffrey L. Arriza,Cary Weinberger,Gail M. Cerelli,Thomas M Glaser,Barbara Handelin,David E. Housman,Ronald M. Evans +7 more
TL;DR: Together the hMR and hGR provide unexpected functional diversity in which hormone-binding properties, target gene interactions, and patterns of tissue-specific expression may be used in a combinatorial fashion to achieve complex physiologic control.
Journal ArticleDOI
Mineralocorticoid action: target tissue specificity is enzyme, not receptor, mediated
TL;DR: The presence of the enzyme 11 beta-hydroxy-steroid dehydrogenase, which converts cortisol and corticosterone, but not aldosterone, to their 11-keto analogs, means that these analogs cannot bind to mineralocorticoid receptors.
Journal ArticleDOI
Antitumor promotion and antiinflammation: Down-modulation of AP-1 (Fos/Jun) activity by glucocorticoid hormone
Carsten Jonat,Hans J. Rahmsdorf,Kun-Koo Park,Andrew C.B. Cato,Stephan Gebel,Helmut Ponta,Peter Herrlich +6 more
TL;DR: Coprecipitation experiments suggest direct AP-1-hormone receptor interaction, which also possibly explains the reverse experiment: overexpression of Fos or Jun inhibits the expression of hormone-dependent genes.
Journal ArticleDOI
Transcriptional interference between c-Jun and the glucocorticoid receptor: Mutual inhibition of DNA binding due to direct protein-protein interaction
Hsin-Fang Yang-Yen,Jean-Claude Chambard,Yu-Lin Sun,Tod Smeal,Thomas J. Schmidt,Jacques Drouin,Michael Karin +6 more
TL;DR: Findings reveal a cross talk between two major signal transduction systems used to control gene transcription in response to extracellular stimuli, and a novel mechanism for transcriptional repression.
Journal ArticleDOI
Crystallographic analysis of the interaction of the glucocorticoid receptor with DNA.
B. F. Luisi,W. X. Xu,Zbyszek Otwinowski,Leonard P. Freedman,Leonard P. Freedman,Keith R. Yamamoto,Paul B. Sigler +6 more
TL;DR: Two crystal structures of the glucocorticoid receptor DNA-binding domain complexed with DNA are reported, which have a globular fold which contains two Zn-nucleated substructures of distinct conformation and function.