癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
HSD11B2 Rabbit pAb
HSD11B2 Rabbit pAb
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- 实验流程
- 背景知识
Application 
| WB, IHC-P, IHC-F, IF |
|---|---|
| Primary Accession | P80365 |
| Reactivity | Human, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 45 KDa |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human HSD11B2 |
| Epitope Specificity | 151-250/405 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | Preservative: 0.02% Proclin300, Constituents: 1% BSA, 0.01M PBS, pH7.4. |
| SUBCELLULAR LOCATION | Microsome. Endoplasmic reticulum. |
| SIMILARITY | Belongs to the short-chain dehydrogenases/reductases (SDR) family. |
| SUBUNIT | Interacts with ligand-free cytoplasmic NR3C2. |
| DISEASE | Defects in HSD11B2 are the cause of apparent mineralocorticoid excess (AME) [MIM:218030]. An autosomal recessive form of low-renin hypertension. It is usually diagnosed within the first years of life and is characterized by polyuria and polydipsia, failure to thrive, hypernatremia, severe hypertension with low renin and aldosterone levels, profound hypokalemia with metabolic alkalosis, and most often nephrocalcinosis. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | 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. [provided by RefSeq, Feb 2010] |
| Other Names | 11-beta-hydroxysteroid dehydrogenase type 2, 11-DH2, 11-beta-HSD2, 1.1.1.-, 11-beta-hydroxysteroid dehydrogenase type II, 11-HSD type II, 11-beta-HSD type II, Corticosteroid 11-beta-dehydrogenase isozyme 2, NAD-dependent 11-beta-hydroxysteroid dehydrogenase, Short chain dehydrogenase/reductase family 9C member 3, HSD11B2 (HGNC:5209) |
|---|---|
| Target/Specificity | Found in placenta, kidney, pancreas, prostate, ovary, small intestine and colon. |
| Dilution | WB=1:500-2000,IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500 |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
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. [provided by RefSeq, Feb 2010]
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