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Validated All-in-One™ qPCR Primer for HSD11B1(NM_001206741.2) Search again
Product ID:
HQP155328
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
11-DH, 11-beta-HSD1, CORTRD2, HDL, HSD11, HSD11B, HSD11L, SDR26C1
Gene Description:
hydroxysteroid 11-beta dehydrogenase 1
Target Gene Accession:
NM_001206741.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
The protein encoded by this gene is a microsomal enzyme that catalyzes the conversion of the stress hormone cortisol to the inactive metabolite cortisone. In addition, the encoded protein can catalyze the reverse reaction, the conversion of cortisone to cortisol. Too much cortisol can lead to central obesity, and a particular variation in this gene has been associated with obesity and insulin resistance in children. Two transcript variants encoding the same protein have been found for this gene. [provided by RefSeq].
Gene References into function
- Effect of cellular differentiation on 11beta-hydroxysteroid dehydrogenase activity in the intestine
- Human adrenal cortex and aldosterone secreting adenomas express both 11beta-hydroxysteroid dehydrogenase type 1 and type 2 genes.
- 11beta-Hydroxysteroid dehydrogenase types 1 and 2 are up- and downregulated in cortisol-secreting adrenal adenomas.
- cultured human ovarian surface epithelium (HOSE) cells express IL-1-responsive 11betaHSD1 mRNA
- There is colocalization of 11beta-HSD1 and GR in the chorionic trophoblast. By binding to GR, glucocorticoids induce the expression of 11beta-HSD1 by a possible intracrine mechanism.
- Acts as dehydrogenase inactivating cortisol to cortisone. 11beta-HSD1 dehydrogenase activity in "uncommitted" omental preadipocytes may provide autocrine mechanism to protect preadipocytes from differentiation, facilitating proliferation.
- May regulate levels of glucocorticoids. Plasma cortisol levels could be predicted by a model incorporating adrenal HSD11B2 and tumor size.
- Higher adipose 11-HSD1 activity is associated with features of metabolic syndrome.
- Mutations in the genes encoding 11beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase interact to cause cortisone reductase deficiency.
- 11beta-HSD1 activity may predict individual susceptibility to glucocorticoid-induced osteoporosis
- idiopathic obesity is associated with transcriptional up-regulation of 11HSD1 in adipose tissue
- glucocorticoids can positively induce 11beta-HSD1 expression in amnion fibroblasts, an effect further strengthened by proinflammatory cytokines.
- increases in 11beta-HSD 1 expression/activity by intrauterine membranes during late gestation may result in increased potential for a local increase in fetal membranes should be considered as an extraadrenal source of cortisol during late gestation.
- REVIEW: role in cortisol metabolism and visceral obesity
- data suggest increased expression of the 11beta-HSD1 gene is associated with metabolic abnormalities in obese women and that increased expression may contribute to increased local conversion of cortisone to cortisol in adipose tissue of obese individuals
- Data report on the in vitro oxysterol-metabolizing properties of human and rodent 11beta-hydroxysteroid dehydrogenase.
- role of the N-terminal region on enzymatic activity and the relevance of 11beta-HSD1 orientation into the endoplasmic reticulum lumen
- P.1088: "...genetic variations in the HSD11B1 gene were associated with Type 2 diabetes mellitus, plasma insulin concentrations and insulin action, independent of obesity."
- Decrease of 11betaHSD1 mRNA abundance and enzyme activity is associated with colorectal cancer
- Decreased 11betaHSD1 activity and expression in obesity may act as a compensatory mechanism to enhance insulin sensitivity through a reduction in tissue-specific cortisol concentrations.
- Hexose-6-phosphate dehydrogenase directly determines the reaction direction of 11beta-Hydroxysteroid dehydrogenase1 in intact cells as an oxoreductase.
- The current study provides additional evidence that variability at the 11[beta]HSD1 gene begets the development of hypertension and that over the years changes in the environment have modified the effect of 11[beta]HSD1 on blood pressure in Pima Indians.
- HIV patients treated with HAART showewd an increase in mRNA of this enzyme in adipose tissue, correlated with insulin resistance.
- crystal structure of human 11beta-hydroxysteroid dehydrogenase type I
- a molecular switch during osteoblast differentiation controls 11beta-Hydroxysteroid dehydrogenase expression and glucocorticoid synthesis
- The portal vein delivers cortisol to the liver, and inhibition of 11HSD1 in visceral adipose tissue may be valuable in ameliorating insulin resistance in obesity.
- monocyte-derived DCs are able to generate cortisol as a consequence of up-regulated 11beta-HSD1 expression. Immature DCs demonstrate selective enhancement of 11beta-HSD1 activity, leading to increased conversion of inactive cortisone to active cortisol.
- 11beta-HSD1 has a role in the metabolism of xenobiotic carbonyl compounds.
- Somatotropin treatment is able to decrease 11beta-HSD1 mRNA and increase 11beta-HSD2 and accordingly may be able to reduce the amount of locally produced cortisol in adipose tissue.
- There was up-regulated expression of 11betaHSD-1 at menstruation and in first trimester decidua.
- ER-lumenal orientation of 11beta-HSD1 is essential for the metabolism of the alternative substrate 7-ketocholesterol (7KC), a major cholesterol oxidation product found in atherosclerotic plaques and taken up from processed cholesterol-rich food.
- cortisol up-regulates 11beta-HSD1 expression through induction of promoter activity, and the effect is enhanced by IL-1beta
- The hydroxyl side chain of Y177 is likely involved with hyrogen bonding with the 3-hydroxy group of A ring of glycyrrhetinic acid.
- is a steroid oxidoreductase able to use and produce 7alpha- and 7beta-hydroxy-DHEA through an oxidoreduction process generating the 7-oxo-DHEA intermediate
- 11HSD1 is altered in a tissue-specific manner with reduced levels in liver but elevated levels in adipose tissue. Some polymorphisms have been demonstrated in intronic and upstream regions of the HSD11B1 gene.
- Results strengthen the importance of 11beta-HSD-1 in obesity and its associated complications and suggest the need of clinical studies with specific 11beta-HSD-1 inhibitors.
- the lack of increase of 11beta-HSD1 expression in Cushing's syndrome could suggest downregulation of the enzyme as a result of long-term overstimulatio
- Results suggest that gene expression modulation by glucocorticoids is under a decisive influence of target cell 11beta-hydroxysteroid dehydrogenase-1 that modulates the intracellular concentration of active glucocorticoids.
- HSD11B1's expression pattern in subcutaneous and omental adipose tissues.
- Y280 is not involved in substrate binding but rather plays a selective role in inhibitor binding. The involvement of Y280 in inhibitor binding depends on the inhibitor chemical structure.
- Presence of both CYP7B1 and 11beta-HSD1 in human skin.
- GRalpha mRNA is reduced in the omental depot with obesity. The novel correlation of 11betaHSD1 with omental fat cell size is independent of obesity.
- skeletal muscle 11beta-HSD1 and 11beta-HSD2 are altered in diabetes, which together may reduce intracellular cortisol generation, potentially conferring metabolic protection
- cellular trafficking of G6P directly regulates 11beta-HSD1 reductase activity and provides a novel link between glucose metabolism and function of the hypothalamo-pituitary-adrenal axis.
- 11beta-HSD1 activity increases with age, and is reduced in obese boys
- These findings support the hypothesis that the oxido-reductase and epimerase activities of 11beta-HSD1 depend on the positioning of the steroid substrates within the active site and may provide insight into its fine structure and mechanism of action.
- In obesity, 11beta-HSD1 is decreased in the liver and increased in adipose tissue. Polymorphisms in the 11beta-HSD1 gene are also associated with components of the metabolic syndrome. Review.
- data suggest a cell-type specific regulation of the 11beta-HSD1 promoter, which is in agreement with existing expression data from animal and human studies
- Data show that normal human kidney contains active 11beta-HSD1 and 11beta-HSD2, and that 11beta-HSD1 co-localizes with COX-2 in proximal tubule cells.
- Data suggest that humoral factors related to metabolic syndrome synergistically enhance hepatic expression of 11beta-hydroxysteroid dehydrogenase type 1 and cause Cushing state in the liver by increasing the intracellular glucocorticoid level.
- no direct effect of estrogen on adipose 11beta-HSD1 was found in liposuctioned adiose tissue
- Type 1 HSD (HSD1) mRNA and reductase activity were mainly expressed within adipocytes and tightly correlated with adipocyte size.
- Variable expression of HSD11B1 in vascular endothelial cells is reported.
- Increased adipose 11beta-HSD1 expression in women may contribute to glucose intolerance.
- relationship between circulating 11beta-HSD1 mRNA levels & cardiovascular risk factors; results suggest decreased expression of 11beta-HSD1 with increased smoking, BMI & length of menopause; increased expression seen with increasing age & alcohol intake
- upregulation of skeletal muscle 11betaHSD1 activity in response to a physiological stressor: abdominal surgery
- Involvement of p38 MAPK in the TNF-alpha-mediated 11beta-HSD1 regulation; TNF-alpha stimulates enzyme activity in vivo.
- Using co-immunoprecipitation experiments with purified H6PDH and 11beta-HSD1, and with cell lysates expressing H6PDH and 11beta-HSD1, we observe direct physical interaction between the two enzymes.