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
11β-Hydroxysteroid Dehydrogenase 1 Transforms 11-Dehydrocorticosterone into Transcriptionally Active Glucocorticoid in Neonatal Rat Heart
TL;DR: The ability of cardiac cells to use both circulating corticosterone and 11-dehydrocorticosterone as a source of glucocorticoid suggests that the heart is under tonic glucocORTicoid control, implying that glucoc Corticoids play important homeostatic roles in the heart.
Journal ArticleDOI
Proinflammatory cytokines inhibit human placental 11beta-hydroxysteroid dehydrogenase type 2 activity through Ca2+ and cAMP pathways.
Irèn Kossintseva,Susan Wong,Edward D. Johnstone,Larry J. Guilbert,David M. Olson,Bryan F. Mitchell +5 more
TL;DR: Proinflammatory cytokines inhibit human placental 11beta-HSD2 activity through a mechanism that involves increased intracellular Ca2+ and inhibition of adenylyl cyclase, which could result in excessive fetal exposure to maternal cortisol.
Journal ArticleDOI
The role of the 11beta-hydroxysteroid dehydrogenase type 2 in human hypertension.
TL;DR: The 11 beta-hydroxysteroid dehydrogenase type 2 (11 PHSD2) enzyme inactivates 11 betahydroxy steroids in sodium-transporting epithelia such as the kidney, thus protecting the nonselective mineralocorticoid receptor (MR) from occupation by cortisol in humans as discussed by the authors.
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11Beta-hydroxysteroid dehydrogenase type 1 in differentiating omental human preadipocytes: from de-activation to generation of cortisol.
TL;DR: It is postulated that 11β-HSD1 dehydrogenase activity in “uncommitted” OM preadipocytes may provide an autocrine mechanism to protect preADipocytes from differentiation, in turn facilitating their proliferation, thus promoting adipogenesis.
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11β-Hydroxysteroid dehydrogenase type 1 inhibition in type 2 diabetes mellitus.
G. Hollis,R. Huber +1 more
TL;DR: In patients with T2DM failing metformin monotherapy, INCB13739 treatment achieves significant reductions in haemoglobin A1c (HbA1c) and fasting plasma glucose (FPG), and when present improves hyperlipidaemia and hypertriglyceridaemia.
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.