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
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Book ChapterDOI
Modulation of glucocorticoid activity by metabolism of steroids in non-lymphoid organs
TL;DR: The adrenal cortex secretes three classes of steroid hormones: mineralocorticoids, androgens and glucoc Corticosterone, but in humans cortisol (i.e. 17α-OH-corticosterone) is more abundant because 17-hydroxylase is expressed in adrenal fasciculata/reticularis cells.
Journal ArticleDOI
Cardiac Hypertrophy and Related Dysfunctions in Cushing Syndrome Patients—Literature Review
TL;DR: In this article , the authors found that hypercortisolemia has been found to cause cardiomyocyte hypertrophy via glucocorticoid receptor activation and tissue-dependent regulation of 11β-hydroxysteroid dehydrogenase type 1.
Journal ArticleDOI
High‐Cortisol States Can Masquerade as the Cardiometabolic Syndrome
Journal ArticleDOI
Apparent mineralocorticoid excess: comprehensive overview of molecular genetics
TL;DR: In this article , the authors provide insights into the molecular genetics of classic and non-classic apparent mineralocorticoid excess and aim to offer a comprehensive overview of this monogenic disease.
Journal ArticleDOI
Effects of HSD11B1 knockout and overexpression on local cortisol production and differentiation of mesenchymal stem cells
Angelique Kragl,Janosch Schoon,Ana Tzvetkova,Christoph Wenzel,Martina Blaschke,Wolfgang Böcker,Heide Siggelkow,Mladen V. Tzvetkov +7 more
TL;DR: A loss- and a gain-of-function model of the cortisol producing enzyme 11β-HSD1 (HSD11B1) to modulate the endogenous glucocorticoid conversion in SCP-1 cells — a model for human mesenchymal stem cells capable of adipogenic and osteogenic differentiation is described.
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.
Journal ArticleDOI
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.
Journal ArticleDOI
Anti-escherichia coli alpha-haemolysin in control and patient sera
Journal ArticleDOI
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.