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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.
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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.

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Citations
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Journal ArticleDOI

The human 11β-hydroxysteroid dehydrogenase type II enzyme: Comparisons with other species and localization to the distal nephron

TL;DR: The notion that 11 beta-HSD2 is an autocrine protector of the mineralocorticoid receptor and that it plays an important role in cardiovascular homeostatic mechanisms is supported.
Journal ArticleDOI

Analysis of the human gene encoding the kidney isozyme of 11β-hydroxysteroid dehydrogenase

TL;DR: 11 beta-Hydroxysteroid dehydrogenase catalyzes the conversion of cortisol to cortisone and may be deficient in the syndrome of apparent mineralocorticoid excess (AME), which was found to be normal in patients of AME.
Journal ArticleDOI

Analysis of the promoter of the NAD + dependent 11β-hydroxysteroid dehydrogenase (HSD11K) gene in JEG-3 human choriocarcinoma cells

TL;DR: Results suggest that the two Spl sites, either alone or in combination, are essential for transcription of the HSD11K gene in JEG-3 cells.
Journal ArticleDOI

Extranuclear localization of endogenous 11beta-hydroxysteroid dehydrogenase-2 in aldosterone target cells.

TL;DR: It is demonstrated that 11betaHSD2 is in the cytoplasmic compartment with no evidence for nuclear localization, which seems ideal for fulfilling its biological function, i.e. the efficient inactivation of intracellular glucocorticoids before they occupy MRs, which are predominantly cytop lasmic in the absence of hormone.
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

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

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.
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