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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.
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.

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Citations
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Journal ArticleDOI

Adamantyl carboxamides and acetamides as potent human 11β- hydroxysteroid dehydrogenase type 1 inhibitors

TL;DR: A series of adamantyl carboxamide and acetamide derivatives were identified, providing potent and selective inhibitors of the therapeutic target human 11β-hydroxysteroid dehydrogenase type 1.
Journal ArticleDOI

Selective toxicity of glycyrrhetinic acid against tumorigenic r/m HM-SFME-1 cells is potentially attributed to downregulation of glutathione

TL;DR: Data highlighting the downregulation of GSH by GA and the efficacy of G SH in ameliorating GA-mediated cytotoxicity support the notion that GSH is involved in the selective toxicity of GA toward tumor cells.
Journal ArticleDOI

A Lower Maternal Cortisol-to-Cortisone Ratio Precedes Clinical Diagnosis of Preterm and Term Preeclampsia by Many Weeks.

TL;DR: A lower maternal serum cortisol-to-cortisone ratio precedes clinical manifestation of PE and preterm FGR by many weeks, despite previous reports of reduced levels of placental 11βHSD2 in these conditions.
Journal ArticleDOI

Molecular docking and structural analysis of cofactor-protein interaction between NAD+ and 11β-hydroxysteroid dehydrogenase type 2

TL;DR: The present study proposes the latest models for 11βHSD2 and its cofactor NAD+, and to the best of the authors' knowledge, this is the first report of a m11β HSD2 model with NAD+.
Dissertation

Prenatal glucocorticoid programming of 11-beta hydroxysteroid dehydrogenase type 2 and erythropoietin in the kidney

TL;DR: This chapter discusses the research evidence for link between low birth weight and later disease and the development of novel approaches to treatment, as well as some of the approaches currently used.
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

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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