Journal ArticleDOI
Cloning and tissue distribution of the human 1 lβ-hydroxysteroid dehydrogenase type 2 enzyme
TLDR
The 11β-hydroxysteroid dehydrogenase (11βHSD) as mentioned in this paper was found to protect the nonselective mineralocorticoid receptor from occupation by glucocorticity, and to modulate access of glucoc Corticoid to glucoc corticoid receptors resulting in protection of the fetus and gonads.About:
This article is published in Molecular and Cellular Endocrinology.The article was published on 1994-11-01. It has received 678 citations till now. The article focuses on the topics: Glucocorticoid receptor & Apparent mineralocorticoid excess syndrome.read more
Citations
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Journal ArticleDOI
Characterization of 11beta-hydroxysteroid dehydrogenase activity and corticosteroid receptor expression in human osteosarcoma cell lines.
Rosemary Bland,CA Worker,BS Noble,L.J. Eyre,Iwona Bujalska,Michael C. Sheppard,Paul M. Stewart,Martin Hewison +7 more
TL;DR: It is postulate that expression of the type 1 and type 2 isoforms of 11beta-HSD in human bone plays an important role in normal bone homeostasis, and may be implicated in the pathogenesis of steroid-induced osteoporosis.
Journal ArticleDOI
Apparent Mineralocorticoid Excess: Genotype Is Correlated With Biochemical Phenotype
Tomoatsu Mune,Perrin C. White +1 more
TL;DR: The biochemical phenotype of the syndrome of apparent mineralocorticoid excess is largely determined by genotype, with the urinary (THF+aTHF)/THE ratio in patients carrying each mutation strongly correlated with in vitro enzymatic activity of the corresponding mutant.
Journal ArticleDOI
Apparent mineralocorticoid excess syndrome: an overview
TL;DR: Substrate excess as seen in Cushing's syndrome and ACTH ectopic production can overwhelm the capacity of 11beta-HSD2 to convert F to E, leading up to an acquired form of AME.
Journal ArticleDOI
Rapid mechanisms of glucocorticoid signaling in the Leydig cell.
Guo-Xin Hu,Qing-Quan Lian,Han Lin,Han Lin,Syed A. Latif,David J. Morris,Matthew P. Hardy,Ren-Shan Ge,Ren-Shan Ge +8 more
TL;DR: Under stress conditions, glucocorticoids have rapid actions to suppress cAMP formation thus to lower testosterone production and 17beta-hydroxysteroid dehydrogenase 3 forms the coupling with 11betaHSD1 which constitutes a rapid mechanism for modulating glucOCorticoid control of testosterone biosynthesis.
Journal ArticleDOI
Insights Into Glucocorticoid-Associated Hypertension.
TL;DR: The association between excess glucocorticoids and hypertension has been much discussed but poorly understood and has the potential to alter both circulating volume and vascular resistance.
References
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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.
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LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR
C. R. W. Edwards,D. Burt,M.A. Mcintyre,E.R. de Kloet,Paul M. Stewart,Lawrence P. Brett,W. Sutanto,Carl Monder +7 more
TL;DR: Findings seem to explain why sodium retention, hypokalaemia, and hypertension develop in subjects with congenital deficiency of 11 beta-OHSD and those in whom the enzyme has been inhibited by liquorice.
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A workbench for multiple alignment construction and analysis.
TL;DR: An interactive program, MACAW (Multiple Alignment Construction and Analysis Workbench), that allows the user to construct multiple alignments by locating, analyzing, editing, and combining “blocks” of aligned sequence segments.
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Anti-escherichia coli alpha-haemolysin in control and patient sera
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Mineralocorticoid activity of liquorice: 11-beta-hydroxysteroid dehydrogenase deficiency comes of age
TL;DR: It is suggested that in both conditions there is a defect in the renal conversion of cortisol to cortisone by 11 beta-OHSD which results in high intrarenal cortisol levels, acting on type 1 mineralocorticoid receptors to cause sodium retention.