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货号: YP-mAb-05496
促销价:

产品介绍

反应种属
Human;Rat;Mouse;
应用范围
WB
抗体类型
单克隆抗体
基因名称(Gene Name)
HSD11B2 HSD11K
蛋白名称
Corticosteroid 11-beta-dehydrogenase isozyme 2 (EC 1.1.1.-) (11-beta-hydroxysteroid dehydrogenase type 2) (11-DH2) (11-beta-HSD2) (11-beta-hydroxysteroid dehydrogenase type II) (-HSD11 type II) (NAD-d
分子量(DA)
44kD
免疫原
Synthesized peptide derived from part region of human protein
特异性
DHI2 Monoclonal Antibody detects endogenous levels of protein.
组成
Liquid in PBS containing 50% glycerol, and 0.02% sodium azide.
来源
Monoclonal, Mouse,IgG
稀释比例
WB 1:500-2000
纯化工艺
The antibody was affinity-purified from mouse antiserum by affinity-chromatography using epitope-specific immunogen.
浓度
1 mg/ml
储存
-20°C/1 year
其他名称
背景
hydroxysteroid 11-beta dehydrogenase 2(HSD11B2) Homo sapiens 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 mine
功能
catalytic activity:An 11-beta-hydroxysteroid + NAD(+) = an 11-oxosteroid + NADH.,disease:Defects in HSD11B2 are the cause of apparent mineralocorticoid excess (AME) [MIM:218030]. AME is a potentially fatal disease characterized by severe juvenile low-renin hypertension, sodium retention, hypokalemia and low levels of aldosterone. It often leads to nephrocalcinosis.,enzyme regulation:Inhibited by glycyrrhetinic acid (derived from liquorice), carbenoloxone and 11-alpha-OH-progesterone.,function:Catalyzes the conversion of cortisol to the inactive metabolite cortisone. Modulates intracellular glucocorticoid levels, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids.,miscellaneous:Consumption of large amounts of liquorice can lead to apparent mineralocorticoid excess and hypertension.,similarity:Belongs to the short-chain dehydrogenases/reductases

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