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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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Steroid disorders in children: congenital adrenal hyperplasia and apparent mineralocorticoid excess.

TL;DR: The research team and laboratories have concentrated on two inherited endocrine disorders, congenital adrenal hyperplasia (CAH) and apparent mineralocorticoid excess, in thier investigations of the pathophysiology of adrenal steroid hormone disorders in children.
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Tissue-specific modulation of mineralocorticoid receptor function by 11β-hydroxysteroid dehydrogenases : an overview

TL;DR: The consequences of cell-specific differences in the coexpression of MR with these proteins need to be further investigated in order to understand the role of this receptor in a given tissue as well as its systemic impact.
Journal ArticleDOI

Exclusion of corticosterone from epithelial mineralocorticoid receptors is insufficient for selectivity of aldosterone action: in vivo binding studies.

J Funder, +1 more
- 01 Dec 1996 - 
TL;DR: Adrenalectomized weanling rats injected with [3H]aldosterone plus excess RU486 show tissue-specific patterns of competition for tracer binding to mineralocorticoid receptors (MR) as evidence that relatively low levels of aldosterone cross the blood-brain barrier and specificity-conferring mechanisms in addition to the exclusion of corticosterone from epithelial MR are required for selective ald testosterone action in sodium homeostasis.
Journal ArticleDOI

11β-Hydroxysteroid Dehydrogenase Complementary Deoxyribonucleic Acid in Rainbow Trout: Cloning, Sites of Expression, and Seasonal Changes in Gonads

TL;DR: The cloned cDNAs encoding rainbow trout 11beta-HSD showed a pattern similar to that of stress-induced serum cortisol levels, but not to serum androgen levels, raising the possibility of a role for rt11beta- HSD in the protection of developing gonads from the inhibitory effects of Stress-induced cortisol.
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Selective regulation of bone cell apoptosis by translational isoforms of the glucocorticoid receptor.

TL;DR: It is shown here that specific, but not all, glucocorticoid receptor isoforms induced apoptosis in human osteosarcoma U-2 OS bone cells, providing new evidence that translational glucoc Torticoid receptors isoforms can elicit distinct glucoc Corticoid responses and may be useful for the development of safe glucocORTicoids with reduced side effects.
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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