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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

Interconversion of cortisol and cortisone in the baboon placenta at midgestation : Expression of 11β-hydroxysteroid dehydrogenase type 1 messenger RNA

TL;DR: It is suggested that the net formation of F from E during transuterine passage in vivo at this stage of gestation results from the 11beta-HSD-1 in the syncytiotrophoblast cells of the baboon placenta.
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Localisation of 11β-Hydroxysteroid Dehydrogenase Type 2 in Mineralocorticoid Receptor Expressing Magnocellular Neurosecretory Neurones of the Rat Supraoptic and Paraventricular Nuclei.

TL;DR: Findings suggest that MNCs in the SON and PVN are aldosterone‐sensitive neurones, and 11β‐HSD2 mRNAs from cDNA libraries derived from single identified MNCS are detected.
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11β-hydroxysteroid dehydrogenase type 2 in zebra finch brain and peripheral tissues

TL;DR: The wide distribution of 11betaHSD2 and MR throughout the songbird brain suggests that concentrations of glucocorticoids may be locally regulated in brain to modulate their actions on MR and possibly also glucOCorticoid receptors (GR).
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Dexamethasone and betamethasone administration during pregnancy affects expression and function of 11β-hydroxysteroid dehydrogenase type 2 in the rat placenta

TL;DR: The data indicate that placental barrier function mediated by 11 beta-HSD2 might be considerably impaired by the antenatal therapy with DXM and BTM, and the discrepancy between expressional and functional studies suggests that sole analysis of expressional changes of 11 Beta-HSSD2 at mRNA and/or protein levels cannot convincingly predict the role of GC treatment on 11beta- HSD2 function in the placental Barrier.
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.
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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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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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