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There are at least two isozymes of the corticosteroid 11-beta-dehydrogenase, a microsomal enzyme complex responsible for the interconversion of cortisol and cortisone. Additionally we are shipping Hydroxysteroid (11-Beta) Dehydrogenase 2 Kits (22) and Hydroxysteroid (11-Beta) Dehydrogenase 2 Proteins (9) and many more products for this protein.
Showing 10 out of 88 products:
Cow (Bovine) Polyclonal HSD11B2 Primary Antibody for WB - ABIN2776772
Subtil-Rodríguez, Millán-Ariño, Quiles, Ballaré, Beato, Jordan: Progesterone induction of the 11beta-hydroxysteroid dehydrogenase type 2 promoter in breast cancer cells involves coordinated recruitment of STAT5A and progesterone receptor to a distal enhancer and polymerase tracking. in Molecular and cellular biology 2008
Human Polyclonal HSD11B2 Primary Antibody for FACS, IHC (p) - ABIN950176
Mericq, Medina, Kakarieka, Márquez, Johnson, Iñiguez: Differences in expression and activity of 11beta-hydroxysteroid dehydrogenase type 1 and 2 in human placentas of term pregnancies according to birth weight and gender. in European journal of endocrinology / European Federation of Endocrine Societies 2009
Infants with the high-risk neurobehavioral profile showed more methylation than infants with the low-risk neurobehavioral profile at CpG3 for NR3C1 (show NR3C1 Antibodies) and less methylation of CpG3 for HSD11B2.
growth potential of fetus related to the 11beta-HSD2 expression in the placenta, and 11beta-HSD2 expression related to the trace metals status of the mother
maternal depression and anxiety may impact on fetal programming by down-regulating HSD11B2, and antidepressant treatment alone is unlikely to protect against this effect.
Data show that glucocorticoid response genes NR3C1 (show NR3C1 Antibodies), ADCYAP1R1 (show ADCYAP1R1 Antibodies) and HSD11B2 were relatively hypomethylated whereas FKBP5 (show FKBP5 Antibodies) was hypermethylated.
No interaction was found between HSD11B2 and exposure during pregnancy, but individuals with the A allele of rs5479 had an increased risk of schizophrenia after exposure at age 3-9 years
11betaHSD2 inhibition suppressed lung tumor growth and invasion in association with increased tissue active glucocorticoid levels, decreased COX-2 (show COX2 Antibodies) expression, inhibition of ERK (show EPHB2 Antibodies) and mTOR (show FRAP1 Antibodies) signaling pathways.
Our work is one of the first comprehensive views of DNA methylation (show HELLS Antibodies) and expression in the placenta for both HSD11B (show HSD11B1 Antibodies) types 1 and 2, linking epigenetic alterations with the regulation of fetal stress and birth weight outcomes.
A novel HSD11B2 functional mutation accounting for an Ala221Gly substitution causes Apparent mineralocorticoid excess. The hypertension phenotype is also epigenetically modulated by HSD11B2 methylation in subjects heterozygous for the mutation
infants with low NR3C1 (show NR3C1 Antibodies) methylation but high HSD11B2 methylation had lower excitability scores; those with high NR3C1 (show NR3C1 Antibodies) methylation but low HSD11B2 methylation had more asymmetrical reflexes
Insulin (show INS Antibodies) reduced the 11beta-HSD2 activity in cancer colon cell lines (HCT116, SW620 and HT-29) at the transcriptional level, in a time and dose dependent manner.
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 (show HSD11B1 Antibodies) 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 (show HAL Antibodies) 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 (show NR3C1 Antibodies) during follicular maturation and atresia: in atretic follicles, expression of 11HSD2 increased in both granulosa cells and theca interna layers
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 (show NR3C2 Antibodies)-dependent pathway.
results show that intestinal epithelial 11ssHSD2 activity contributes to increased COX-2 (show COX2 Antibodies) expression in Apc (show APC Antibodies)+/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 (show HELLS Antibodies) 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 (show AVPR2 Antibodies).
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.
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