Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Alle Spezies anzeigen
Weitere Synonyme anzeigen
Wählen Sie die Spezies und Applikation aus
anti-Mouse (Murine) Antikörper:
anti-Rat (Rattus) Antikörper:
Sie gelangen zu unserer vorgefilterten Suche.
Human Polyclonal HSD11B2 Primary Antibody für IF (p), IHC (p) - ABIN701680
Ding, Shi, Han, Cui: Regulation of glucocorticoid-related genes and receptors/regulatory enzyme expression in intrauterine growth restriction filial rats. in Life sciences 2016
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.
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 (zeige SHH Antikörper) 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 (zeige RACGAP1 Antikörper) regulates 11beta-HSD2 expression, mineralocorticoid receptor (zeige NR3C2 Antikörper) activation, and mineralocorticoid receptor (zeige NR3C2 Antikörper)-mediated pro-fibrotic signaling.
enhancer of zeste homolog 2 (EZH2 (zeige EZH2 Antikörper)) accounts for the silence of 11beta-HSD2 expression via trimethylation of histone H3 (zeige HIST3H3 Antikörper) 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 (zeige HELLS Antikörper) in HSD11B2 and FKBP5 (zeige FKBP5 Antikörper) are seen in a minority of bisulfite sequencing clones, these epigenetic changes, and functional consequences, may affect subpopulations of placental cells.
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 (zeige HSD11B1 Antikörper) 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 (zeige HAL Antikörper) 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.
investigation of expression for 11HSD1, 11HSD2, and glucocorticoid receptor (zeige NR3C1 Antikörper) during follicular maturation and atresia: in atretic follicles, expression of 11HSD2 increased in both granulosa cells and theca interna layers
Kidney-specific deficiency of 11beta-HSD2 leads to Salt-dependent Hypertension, which is attributed to mineralocorticoid receptor (zeige NR3C2 Antikörper)-epithelial sodium channel-Na(+)-Cl(-) cotransporter (zeige SLC12A3 Antikörper) activation in the kidney.
Nr3c2 (zeige NR3C2 Antikörper) has a role in mouse skin development in a process that involves HSD11B1 (zeige HSD11B1 Antikörper)/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 (zeige NR3C2 Antikörper)-dependent pathway.
11betaHSD2 inhibition suppressed lung tumor growth and invasion in association with increased tissue active glucocorticoid levels, decreased COX-2 (zeige COX2 Antikörper) expression, inhibition of ERK (zeige EPHB2 Antikörper) and mTOR (zeige FRAP1 Antikörper) signaling pathways.
results show that intestinal epithelial 11ssHSD2 activity contributes to increased COX-2 (zeige COX2 Antikörper) expression in Apc (zeige APC Antikörper)+/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 (zeige HELLS Antikörper) 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 (zeige AVPR2 Antikörper).
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