Rabbit Anti-HSD11B2/FITC Conjugated antibody

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Corticosteroid 11 beta dehydrogenase isozyme 2; 11 beta HSD2; 11 beta hydroxysteroid dehydrogenase type 2; 11 DH2; AME; AME1; HSD11K; HSD2; Hydroxysteroid 11 beta dehydrogenase 2; Hydroxysteroid 11 beta dehydrogenase isoenzyme 2; NAD dependent 11 beta hyd

Cat:

SL3618R-FITC

Species Reactivity：

Mouse,Rat,Horse,(predicted: Human,Dog,)

Immunogen：

KLH conjugated synthetic peptide derived from human HSD11B2

Format：

Lyophilized or Liquid

Storage instructions：

Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of ant

Buffer：

0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.

Concentration：

1mg/ml

Clonality：

Polyclonal

Isotype：

IgG

Applications：

IF=1:50-200not yet tested in other applications.optimal dilutions/concentrations should be determined by the end user.

Host：

Rabbit

Calculated MW：

45kDa

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Unit:

Price: $596.00

Product PDFs

Datasheet: Down Datasheet

Other Information
Citations
Protein Attributes
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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]

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.

Subunit:
Interacts with ligand-free cytoplasmic NR3C2.

Subcellular Location:
Microsome. Endoplasmic reticulum.

Tissue Specificity:
Found in placenta, kidney, pancreas, prostate, ovary, small intestine and colon.

Similarity:
Belongs to the short-chain dehydrogenases/reductases (SDR) family.

Database links:

Entrez Gene: 282434 Cow

Entrez Gene: 3291 Human

Entrez Gene: 15484 Mouse

Entrez Gene: 396948 Pig

Entrez Gene: 25117 Rat

Omim: 23630 Human

SwissProt: O77667 Cow

SwissProt: P80365 Human

SwissProt: P51661 Mouse

SwissProt: P51976 Rabbit

SwissProt: P50233 Rat

SwissProt: P50168 Sheep

Unigene: 1376 Human

Unigene: 5079 Mouse

Unigene: 10186 Rat

Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

[DISEASE] Defects in HSD11B2 are the cause of apparent mineralocorticoid excess (AME) [MIM:23630]. 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.

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