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Validated All-in-One™ qPCR Primer for HSD11B2(NM_000196.3) Search again
Product ID:
HQP009063
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AME, AME1, HSD11K, HSD2, SDR9C3
Gene Description:
hydroxysteroid 11-beta dehydrogenase 2
Target Gene Accession:
NM_000196.3(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.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- Effect of cellular differentiation on 11beta-hydroxysteroid dehydrogenase activity in the intestine
- effect of ATP on activity in human placental microsomes
- in vivo footprinting of promoter and cell-specific regulation by Sp1 and Sp3
- Weak associations between the HSD11B2 gene, type 1 diabetes mellitus and nephropathy.
- Human adrenal cortex and aldosterone secreting adenomas express both 11beta-hydroxysteroid dehydrogenase type 1 and type 2 genes.
- chenodeoxycholic acid and deoxycholic acid, by inhibiting 11 beta HSD2, mediate cortisol-dependent nuclear translocation and transcriptional activation of Mineralocorticoid receptor
- 11beta-Hydroxysteroid dehydrogenase types 1 and 2 are up- and downregulated in cortisol-secreting adrenal adenomas.
- The expression of 11 beta-hydroxysteroid dehydrogenase type 2 is induced during trophoblast differentiation: effects of hypoxia.
- first report to suggest that 11 beta-hydroxysteroid dehydrogenase 2 is O(2) dependent in first and third trimester placenta during human gestation
- In small preterm infants, reduced placental 11 beta-HSD2 function is asociated with low relative birth weight and severe fetal distress.
- Nonfunctioning adenomas and those causing preclinical and overt Cushing's syndrome may represent a continuum with clinical manifestations depending mainly on tumor size and HSD11B2 expression levels.
- determination of abnormal expression in pituitary adenomas
- 11 beta-Hydroxysteroid dehydrogenase type 2 (11 beta-HSD2) plays a crucial role in converting hormonally active cortisol to inactive cortisone, thereby conferring specificity on the mineralocorticoid receptor. Review.
- Homozygous mutation in exon 4 Asp223Asn changed the enzyme's surface electrostatic potential affecting the cofactor and substrate enzyme-binding capacity.
- Late-onset apparent mineralocorticoid excess caused by novel compound heterozygous mutations in the HSD11B2 gene.
- Ang II decreases activity of 11beta-HSD2 by AT2 receptor- and MAPK-dependent mechanism. Decreased activity of 11beta-HSD2 increases intracellular availability of cortisol. May be relevant for pathogenesis of hypertension and preeclampsia.
- An increase in the expression of 11 beta-HSD2 may result in faster glucocorticoid breakdown in lung cells in patients with acute respiratory distress syndrome (ARDS).
- results suggest that renal 11-hydroxysteroid dehydrogenase 2 is a main factor controlling the equilibrium of plasma cortisol and cortisone concentrations in the periphery
- Patients with essential hypertension and without any biological evidence of aldosterone excess have an overall significant 39% reduction in ex vivo HSD2 catalytic activity in sweat gland ducts, as compared with normotensive subjects.
- Decrease of 11betaHSD2 mRNA abundance and enzyme activity is associated with colorectal cancer
- The antiproliferative effects of glucocorticosteroids were reversed and total cell growth boosted by overexpression of 11beta-HSD2. The increase in cell proliferation was attained by low 11beta-HSD2 overexpression.
- These results indicate a role for DNA methylation in 11 beta-hydroxysteroid dehydrogenase type 2 gene repression and suggest an epigenetic mechanism affecting this gene causally linked with hypertension.
- 11beta-HSD2 is an additional target for PPAR delta, which may regulate human placental function
- Critical role of 11betaHSD2 for ensuring selectivity of the mineralocarticoid receptors in the distal nephron
- hypertensives with suppressed renin activity may have an impairment in the cortisol inactivation catalyzed by the enzyme 11betaHSD2, which could be associated with the length of CA-repeat microsatellite in intron 1 of the HSD11B2 gene
- Reduced renal 11beta-HSD2 expression may lead to occupancy of the MR by glucocorticoids such as cortisol and may contribute to the increased sodium retention seen in patients with impaired renal function
- Study identifies placental 11 beta-HSD2 as a novel molecular target of cadmium.
- The reduced placental 11beta-HSD2 in fetal growth restriction is not due to intrinsic abnormalities in trophoblast cells, but likely a result of extrinsic factors associated with FGR.
- lung inflammation reduces local glucocorticoid breakdown and augments glucocorticoid action in the lung by down-regulating 11beta-HSD2 via multiple mechanisms
- 11BetaHSD-2 and GR were expressed across the mensrual cycle.
- missense mutations in HSD11B2 do not substantially contribute to essential hypertension in Japanese
- The 3 most significantly overexpressed genes were in rheumatoid arthritis were laeverin, 11beta-hydroxysteroid dehydrogenase type 2 (a steroid pathway enzyme), and cysteine-rich, angiogenic inducer 61 (a known angiogenic factor).
- Data show that protein kinase A pathway activators such as arginine vasopressin induce, and protein kinase C pathway activators repress the expression of 11beta-hydroxysteroid dehydrogenase type 2 in human renal epithelial cells.
- renal 11beta-hydroxysteroid dehydrogenase type 2 is an important regulatory factor of renal Na and K
- Data show that type 2 1beta-hydroxysteroid dehydrogenase activity in ovarian cancer specimens is significantly higher than enzyme activity measured in normal post-menopausal ovarian tissue.
- Data show that 11-beta hydroxysteroid dehydrogenase type 2 (HSD2) protein and activity levels increase with differentiation of alveolar type II cells, and that HSD2 protein levels are regulated by 17-beta estradiol in male fetal lung tissue.
- skeletal muscle 11beta-HSD1 and 11beta-HSD2 are altered in diabetes, which together may reduce intracellular cortisol generation, potentially conferring metabolic protection
- conclude that the mechanism of glucocorticoid-induced HSD11B2 expression is mainly mediated by cooperation between glucocorticoid receptor and nuclear factor 1 on the HSD11B2 promoter
- The effect of LOX metabolites on HSD11B2 is mediated by their stimulation of endogenous progesterone output.
- A role for an attenuated placental as well as fetal 11beta-HSD2 in the pathogenesis of intrauterine growth restriction.
- 11 beta-hydroxysteroid dehydrogenase 2 gene promoter epigenetic control is related to human hypertension
- 11beta-HSD2 gene expression in breast cancer cells by progesteron was studied.
- Cortisol inactivation and HSD2 mRNA expression (expressed in stromal cells) were higher in omentum suggesting higher cortisol turnover.
- Our study indicates MR and 11beta-HSD2 are both sensitive and specific markers of the distal nephron and its related neoplasms (chromophobe renal cell carcinomas and oncocytomas).
- In obesity, the kidney appears to intensify its supply of the direct substrate cortisone for extrarenal 11beta-HSD1, which may fuel visceral adiposity and insulin resistance.
- Variable expression of HSD11b1 in vascular endothelial cells is reported.
- Data show that plasma DNA and mRNA for 11beta-hydroxysteroid dehydrogenase type II is significantly lower in hypertensive patients than in healthy subjects.
- There may be a mechanism other than that via 11betaHSD2 for causes of impaired negative feedback action by glucocorticoids in subclinical Cushing's and Cushing's disease.