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
Citations
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Journal ArticleDOI
Expression of 11β-hydroxysteroid-dehydrogenase 2 in Sertoli cells of boar testes
Rolf Claus,Markus Lacorn,Harald Welter,Oksana Lekhkota,Nina Messe,Anna Wagner,Martin Bergmann +6 more
TL;DR: It is concluded that the expression of 11beta-HSD2 in several types of cells forms consecutive lines of defense to protect spermatogonia against glucocorticoid-induced apoptosis.
Book ChapterDOI
Secretion and Metabolism of Steroids in Primate Mammals During Pregnancy
TL;DR: Estrogen has been implicated in the cascade of events that initiate the process of labor, and cortisol produced by the fetal adrenal gland has a critical role in the maturation of the lung and other organ systems in the developing fetus.
Journal ArticleDOI
Zearalenone Inhibits Rat and Human 11β-Hydroxysteroid Dehydrogenase Type 2
Linxi Li,Xiaolong Wu,Hongguo Guan,Baiping Mao,Huang Wang,Xiaohuan Yuan,Yanhui Chu,Jianliang Sun,Ren-Shan Ge +8 more
TL;DR: It is observed that zearalenone is a selective inhibitor of HSD11B2, implying that this agent may cause excessive glucocorticoid action in local tissues such as kidney and placentas.
Journal ArticleDOI
Enhanced 11beta-hydroxysteroid dehydrogenase type 1 activity in stress adaptation in the guinea pig.
Marcus Quinkler,H Troeger,E. Eigendorff,C Maser-Gluth,A Stiglic,Wolfgang Oelkers,Volker Bähr,S. Diederich +7 more
TL;DR: The enhanced reductase activity of the hepatic and renal 11beta-HSD-1 is apparently caused by cortisol or other ACTH-dependent steroids rather than by ACTH itself, which may be an important fine regulation of the glucocorticoid tonus for stress adaptation in every organ.
Journal ArticleDOI
Apparent mineralocorticoid excess, 11β hydroxysteroid dehydrogenase and aldosterone action: Closing one loop, opening another
TL;DR: Although the sodium retention characteristic of AME can thus be explained by absent or very reduced levels of renal 11 betaHSD2 activity, whether or not the enzymatic defect contributes to the elevated blood pressure by mechanisms other than sodium retention remains to be determined.
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.