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>   首页   >   产品   >   一抗   >   其他   >   HSD11B2 Rabbit pAb   

HSD11B2 Rabbit pAb

     
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, IHC-P, IHC-F, IF
Primary Accession P80365
Other Accession P80365
Host Rabbit
Clonality Polyclonal
Calculated MW 44127 Da
Physical State Liquid
Immunogen Recombinant human HSD11B2 protein
Isotype IgG
Purity affinity purified by Protein A
Buffer 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
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]
Additional Information
Gene ID 3291
Other Names AME; AME1; HSD11K; HSD2; SDR9C3; 11HSD2; DHI2_BOVIN; HSD11B2; 11-DH2; 11-beta-HSD2; Corticosteroid 11-beta-dehydrogenase isozyme 2; NAD-dependent 11-beta-hydroxysteroid dehydrogenase; 1.1.1.-; DHI2_HUMAN; 11-beta-hydroxysteroid dehydrogenase type II (11-HSD type II | 11-beta-HSD type II); Short chain dehydrogenase/reductase family 9C member 3; DHI2_MOUSE; DHI2_RABIT; 11beta-OHSD type 2; DHI2_RAT; DHI2_SHEEP; hydroxysteroid 11-beta dehydrogenase 2; hydroxysteroid (11-beta) dehydrogenase 2; short chain dehydrogenase/reductase family 9C, member 3
Dilution WB=1:500-2000,IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500
StorageStore 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.

Protein Information
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:23685396, 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:23685396, 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). Catalyzes the conversion of 7-beta-hydroxycholesterol into 7- ketocholesterol (7-oxocholesterol), a precursor of 7-keto,27- hydroxycholesterol, which activates smoothened (SMO) and the smoothened signaling pathway (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).
Research Areas
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