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The presence and localization of glucocorticoid receptors and 11beta-hydroxysteroid dehydrogenase type 1 (HSD11beta) in equine epididymal and testicular tissue with special regard to sexual maturation are reported.
Sequence defects (16q22.1) cause Monogenic Hypertension Syndrome in children (with muscle weakness in severe forms)as result of apparent mineralocorticoid excess.
High systemic 11beta-HSD2 activity in preeclampsia but not in intrauterine growth retardation suggests an increased cortisol deactivation in maternal tissue in preeclampsia rather than in the placenta.
Analyses demonstrated a trend in the association between maternal trait anxiety and depression symptoms with placental gene expression of NR3C1. We found a significant interaction with maternal ethnicity. In Caucasians only, prenatal trait anxiety and depressive symptoms were associated with an increase in placental NR3C1 expression, and prenatal life events were associated with a down regulation of HSD11B2
mutations that allow the formation of an inactive dimer, alter substrate/coenzyme binding, or impair structural stability of HSD11B2 yield severe apparent mineralocorticoid excess (AME). In contrast, mutations that cause an indirect disruption of substrate binding or mildly alter intramolecular interactions result in type 2 AME.
Six sequence variations were observed. Four mutations were indicated in the coding region of HSD11B2 and the other two in 3'-UTR. Two SNPs: c.468C > A and c.534G > A were found to be in total disequilibrium. High variability in HSD11B2 sequence was indicated in the study population, but the relevance of observed SNPs to gestational hypertension or pre-eclampsia development was not confirmed.
the role of 11beta-HSD2 in determining birth weight
SUMOylation of 11beta-HSD2 at residue K266 modulates cortisol-mediated MR nuclear translocation independently of effects on transactivation.
11beta-HSD2 activity is not reduced in patients with drug resistant hypertension, suggesting that variation in the conversion of cortisol to cortisone does not contribute to development of antihypertensive treatment resistance.
abundantly localized in syncytial layer of the chorionic villi and the decidual epithelium
The data demonstrate for the first time that 11b- HSD2 plays a key role in the pathophysiology of malignant epidermal cells.
DNA sequence analysis of affected members of Apparent mineralocorticoid excess family revealed homozygous c.799A>G mutations within exon 4 of HSD11B2, corresponding to a p.T267A mutation of 11betaHSD2.
activation of Hedgehog signaling is crucial for the upregulation and maintenance of 11beta-HSD2 expression in placenta
Reciprocal regulation of the glucocorticoid metabolizing enzymes, 11beta-hydroxysteroid dehydrogenase types 1 and 2, is associated with steroid-responsiveness and disease remission in childhood nephrotic syndrome.
Rac1 GTPase regulates 11beta-HSD2 expression, mineralocorticoid receptor activation, and mineralocorticoid receptor-mediated pro-fibrotic signaling.
enhancer of zeste homolog 2 (EZH2) accounts for the silence of 11beta-HSD2 expression via trimethylation of histone H3 lysine 27 at the promoter of the 11beta-HSD2 gene.
Sensitivity to glucocorticoids did not appear to be mediated by changes in the expression of the beta variant of the glucocorticoid receptor or the 11-beta hydroxysteroid dehydrogenase 2 isozyme.
Review of the role of HSD11B2 in pregnancy complications, fetal diseases, and later life morbidity.
Since increased DNA methylation in HSD11B2 and FKBP5 are seen in a minority of bisulfite sequencing clones, these epigenetic changes, and functional consequences, may affect subpopulations of placental cells.
significant positive correlation between DNA methylation of 11beta-HSD2 CpG 1 in infants and maternal sensitivity.
The 11beta-HSD2 expression decreased in pre-eclamptic women of Chinese Han ethnicity, but was not interrelated with the promoter methylation status.
These results indicate that the effects of maternal protein restriction on placental 11beta-HSD2 expression are gender-dependent in the pig, and thyroid hormones may be involved in such effects.
Postnatal ontogeny of 11beta-HSD2 gene expression is described for the first time in stress-related brain regions of domestic pigs at 7, 21, and 35 days of age.
concluded that the 11beta-hydroxysteroid dehydrogenase (11beta-HSD1 and 2) system is involved in the regulation of cortisol activity in the testis and thus in the regulation of spermatogenesis
Effects of age, weaning and/or social isolation on the expression of genes regulating HSD11B2.
The expression of 11beta-HSD2 in several types of cells forms consecutive lines of defense may protect spermatogonia against glucocorticoid-induced apoptosis.
11beta-HSD type 2, which is abundantly expressed, plays important roles in cortisol inactivation in pig Leydig cells.
The amount of 11beta-HSD 2 in germ cells was greatest at birth, decreased thereafter and was absent after Week 3.
Data show that in the testis, caput epididymidis and bulbourethral gland of the immature pig, 11betaHSD1 and 2 catalyse inactivation of cortisol, supporting a role in limiting local actions of glucocorticoids within these tissues prior to puberty.
investigation of expression for 11HSD1, 11HSD2, and glucocorticoid receptor during follicular maturation and atresia: in atretic follicles, expression of 11HSD2 increased in both granulosa cells and theca interna layers
A subset of HSD2 neurons may promote the dysphoric, anorexic, and anhedonic symptoms of hyperaldosteronism via AgRP-inhibited relay neurons in the parabrachial complex.
Kidney-specific deficiency of 11beta-HSD2 leads to Salt-dependent Hypertension, which is attributed to mineralocorticoid receptor-epithelial sodium channel-Na(+)-Cl(-) cotransporter activation in the kidney.
Nr3c2 has a role in mouse skin development in a process that involves HSD11B1/HSD11B2
Reduced brain 11betaHSD2 promotes a hunger for salt and salt sensitivity. 11betaHSD2-positive neurons integrate salt appetite and the blood pressure response to dietary sodium through a mineralocorticoid receptor-dependent pathway.
11betaHSD2 inhibition suppressed lung tumor growth and invasion in association with increased tissue active glucocorticoid levels, decreased COX-2 expression, inhibition of ERK and mTOR signaling pathways.
placental 11bHSD2 expression is significantly reduced in pregnancies complicated by intrahepatic cholestasis of pregnancy.
results show that intestinal epithelial 11ssHSD2 activity contributes to increased COX-2 expression in Apc+/min intestinal adenomas and that 11ssHSD2 deficiency in intestinal epithelial cells suppresses adenoma development and growth
11beta-hydroxysteroid dehydrogenase-2 is a cortisol-inactivating enzyme with a role in keratinocyte cell proliferation and basal cell proliferation
Reduced 11beta-hydroxysteroid dehydrogenase type 2 causes salt sensitivity of blood pressure because of impaired renal natriuretic capacity.
findings implicate DNA methylation as a mechanism by which prenatal stress alters HSD11B2 gene expression
This study found that 11beta-hydroxysteroid dehydrogenase type 2 knockout mice develop nephrogenic diabetes insipidus.
evidence for a weak or absent expression of neonatal renal 11betaHSD2 that is conserved among species
HSD2 inhibition and increasing corticosterone adult physiological levels both can independently upregulate neural progenitor cell apoptosis in the perinatal period.
11beta-HSD2 plays no role in acute inflammatory responses
Prenatal exposure to ethanol reduced expression of placental 11beta-HSD-2.
Ligand-receptor interaction between triterpenoids and the 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) enzyme predicts their toxic effects against tumorigenic r/m HM-SFME-1 cells.
Reduced activity of 11betaHSD2 causes salt sensitivity of blood pressure
The activation of mineralocorticoid receptors in mice deficient in Apolipoprotein E and 11beta-hydroxysteroid dehydrogenase type 2 and subsequent athersclerosis are reported.
Transgenic (col1A1) Col3.6-HSD2 mice showed a low bone mass phenotype, with decreased ex vivo osteogenesis, which strengthens the concept that endogenous glucocorticoid signaling is required for optimal bone mass acquisition
There are at least two isozymes of the corticosteroid 11-beta-dehydrogenase, a microsomal enzyme complex responsible for the interconversion of cortisol and cortisone. The type I isozyme has both 11-beta-dehydrogenase (cortisol to cortisone) and 11-oxoreductase (cortisone to cortisol) activities. The type II isozyme, encoded by this gene, has only 11-beta-dehydrogenase activity. In aldosterone-selective epithelial tissues such as the kidney, the type II isozyme catalyzes the glucocorticoid cortisol to the inactive metabolite cortisone, thus preventing illicit activation of the mineralocorticoid receptor. In tissues that do not express the mineralocorticoid receptor, such as the placenta and testis, it protects cells from the growth-inhibiting and/or pro-apoptotic effects of cortisol, particularly during embryonic development. Mutations in this gene cause the syndrome of apparent mineralocorticoid excess and hypertension.
hydroxysteroid (11-beta) dehydrogenase 2
, corticosteroid 11-beta-dehydrogenase isozyme 2
, 11 beta-hydroxysteroid dehydrogenase type 2
, -HSD11 type II
, 11-beta-hydroxysteroid dehydrogenase type 2
, 11-beta-hydroxysteroid dehydrogenase type II
, NAD-dependent 11-beta-hydroxysteroid dehydrogenase
, short chain dehydrogenase/reductase family 9C member 3
, 11-beta hydroxysteroid dehydrogenase
, hydroxysteroid 11-beta dehydrogenase 2
, 11-beta-hydroxysteroid dehydrogenase 2
, Hydroxysteroid dehydrogenase, 11 beta type 2