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。
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HSD11B2 Rabbit pAb
HSD11B2 Rabbit pAb
- 产品详情
- 实验流程
- 背景知识
Application 
| WB, IHC-P, IHC-F, IF |
|---|---|
| Primary Accession | P80365 |
| Reactivity | Human, Mouse, Rat |
| Predicted | Dog, Horse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 44127 Da |
| 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] |
| Gene ID | 3291 |
|---|---|
| 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. |
| Name | HSD11B2 (HGNC:5209) |
|---|---|
| Function | Catalyzes the conversion of biologically active 11beta- hydroxyglucocorticoids (11beta-hydroxysteroid) such as cortisol, to inactive 11-ketoglucocorticoids (11-oxosteroid) such as cortisone, in the presence of NAD(+) (PubMed:10497248, PubMed:12788846, PubMed:17314322, PubMed:22796344, PubMed:27927697, PubMed:30902677, PubMed:33387577, PubMed:7859916, PubMed:8538347). Functions as a dehydrogenase (oxidase), thereby decreasing the concentration of active glucocorticoids, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids (PubMed:10497248, PubMed:12788846, PubMed:17314322, PubMed:33387577, PubMed:7859916). Plays an important role in maintaining glucocorticoids balance during preimplantation and protects the fetus from excessive maternal corticosterone exposure (By similarity). Catalyzes the oxidation of 11beta-hydroxytestosterone (11beta,17beta-dihydroxyandrost-4-ene-3-one) to 11-ketotestosterone (17beta-hydroxyandrost-4-ene-3,11-dione), a major bioactive androgen (PubMed:22796344, PubMed:27927697). Catalyzes the conversion of 11beta-hydroxyandrostenedione (11beta-hydroxyandrost- 4-ene-3,17-dione) to 11-ketoandrostenedione (androst-4-ene-3,11,17- trione), which can be further metabolized to 11-ketotestosterone (PubMed:27927697). Converts 7-beta-25-dihydroxycholesterol to 7-oxo-25- hydroxycholesterol in vitro (PubMed:30902677). 7-beta-25- dihydroxycholesterol (not 7-oxo-25-hydroxycholesterol) acts as a ligand for the G-protein-coupled receptor (GPCR) Epstein-Barr virus-induced gene 2 (EBI2) and may thereby regulate immune cell migration (PubMed:30902677). May protect ovulating oocytes and fertilizing spermatozoa from the adverse effects of cortisol (By similarity). |
| Cellular Location | Microsome. Endoplasmic reticulum |
| Tissue Location | Expressed in kidney, placenta, pancreas, prostate, ovary, small intestine and colon, and in lower levels in the spleen and testis (PubMed:7859916). At midgestation, expressed at high levels in placenta and in fetal kidney and, at much lower levels, in fetal lung and testis (PubMed:8530071). |
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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