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
Cortisol metabolism in healthy young adults: sexual dimorphism in activities of A-ring reductases, but not 11beta-hydroxysteroid dehydrogenases
TL;DR: It is concluded that sexual dimorphism in cortisol metabolite excretion is attributable to less A-ring reduction of cortisol in women, rather than less reactivation of cortisone to cortisol by 11betaHSD1.
Journal ArticleDOI
Molecular Basis for Hypertension in the “Type II Variant” of Apparent Mineralocorticoid Excess
A. Li,R. Tedde,Zygmunt S. Krozowski,A. Pala,K. Li,Cedric H.L. Shackleton,Franco Mantero,Mario Palermo,Paul M. Stewart +8 more
TL;DR: In an extensive consanguineous Sardinian pedigree affected with "type II" AME, a novel homozygous point mutation (C945T) was found in the human 11beta-HSD2 gene in four affected individuals.
Journal ArticleDOI
Regulation of 11beta-hydroxysteroid dehydrogenase type 2 by progesterone, estrogen, and the cyclic adenosine 5'-monophosphate pathway in cultured human placental and chorionic trophoblasts.
TL;DR: It is concluded that both progesterone and estrogen are inhibitors of 11beta-HSD2 activity in term human placenta in vitro and levels of 11 beta-HSDs activity and mRNA are increased by activation of the cAMP pathway.
Journal ArticleDOI
11beta-hydroxysteroid dehydrogenase type 1 inhibitors: a review of recent patents.
TL;DR: This review covers the recent 11β-HSD1 patent literature and clinical activity ranging from late 2007 through the end of 2008, as a number of structural classes have been reported by several pharmaceutical companies over the past 16 months.
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11 beta-hydroxysteroid dehydrogenase type 1 is a predominant 11 beta-reductase in the intact perfused rat liver
TL;DR: The substantial concentrations of plasma 11-DHC as substrate suggest that 11 beta-HSD-1 activity and its potential selective inhibition could modify glucocorticoid action in vivo.
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.
Journal ArticleDOI
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.