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
The 11β-Hydroxysteroid dehydrogenase enzymes: perspectives and paradoxes.
Journal ArticleDOI
Potential role of 11 beta-hydroxysteroid dehydrogenase in human trophoblast-endometrial interactions.
F. Arcuri,Carl Monder,Stefania Battistini,V. Hausknecht,Charles J. Lockwood,Frederick Schatz +5 more
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Expression of 11β-hydroxysteroid dehydrogenase isoforms in canine adrenal glands treated with trilostane.
TL;DR: Findings suggest that trilostane may have an effect on 11β-HSD activity in canine adrenal glands.
Journal ArticleDOI
The syndrome of apparent mineralocorticoid excess and deficiency of 11 β‐hydroxysteroid dehydrogenase
TL;DR: Two carefully documented new cases of the syndrome of apparent mineralocorticoid excess are described and several other observations highlighted in this report required explanation to complete understanding of SAME, and any possible relationship with more mundane forms of hypertension.
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The hypertensive patient with hypokalaemia: the search for hyperaldosteronism.
TL;DR: This index provides a semi-quantitative assessment of the apparent transtubular potassium concentration gradient in the major distal nephron segment, where potassium is secreted and is probably a poor re¯ection of aldosterone action.
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.