11-Beta-hydroxysteroid dehydrogenase (11b-HSD) is a microsomal short chain dehydrogenase/reductase (SDR) which catalyzes the inter-conversion of biologically active glucocorticoid (cortisol in human and corticosterone in rats and mice) and inactive glucocorticoid (cortisone and 11-dehydrocorticosterone).
Two tissue specific isoforms (11b-HSD1 and 11b-HSD2) of 11b-HSD with two different functions regarding glucocorticoid availability, have been identified.
The decreased 11-beta-hydroxy oxidation of cortisol results in Apparent Mineralocorticoid Excess (AME) disorder which is manifested by hypertension, hypokalemia, low plasma renin activity, and responsiveness to spironolactone.
AME is principally a disorder of juveniles and children with this condition oxidize cortisol to cortisone poorly but carry out the reverse process unimpaired.
AME arises from mutations in the 11-beta-HSD2 gene.
The glucocorticoids can be produced locally by 11beta-HSD1 and increased visceral accumulation of glucocorticoids results in visceral obesity, insulin resistant diabetes, hyperlipidemia and hyperphagia.
11betaHSD-1 (variously termed as HSD11L; mouse, 292 aa, rat 287 aa, human 292 aa) is a ~35kD glycosylated membrane-protein, oriented into the lumen of endoplasmic reticulum.
This isoform is the sole 11b-reductase in the body and exerts two separate enzymatic activities: 11-beta-dehydrogenase (cortisol to cortisone) and 11-oxoreductase (cortisone to cortisol) in vitro.
In vivo, it acts mainly as reductase producing active cortisol.
The enzyme also plays an important role in xenobiotic carbonyl compound detoxification processes.
11b-HSD1 is expressed in a wide array of tissues, with highest level in Liver and adipose tissues.
The increased adipocyte 11b-HSD1 is a common mechanism for visceral obesity and metabolic syndrome.
Although the deficiency in 11b-HSD1 activity is not related to AME, it results in a syndrome characterized by an increased adrenocorticotropic hormone (ACTH)-driven androgen production.
In mouse, the over-all aa sequence of 11b-HSD1 is approximately 18% identical to that of 11b-HSD2.
Applications:Suitable for use in ELISA.
Western Blot, though not tested, may potentially be used as an application.
Other applications not tested.
Recommended Dilution:Western Blot: 1:1000-1:5000 using ECLELISA: 1:10,000-1:100,000.
Use 50-100ng of control peptide
Optimal dilutions to be determined by the researcher.
Control Peptide: H9117-70
Storage and Stability:May be stored at 4°C for short-term only.
For long-term storage, store at -20°C.
Aliquots are stable for at least 12 months at -20°C.
For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
Further dilutions can be made in assay buffer.
仕様
Size:100ul
Host:rabbit
Source Antibody:mouse
Grade:Serum
Purity:Serum
Form:Supplied as a liquid in PBS, 0.05% sodium azide, 40% glycerol.
Specificity:Recognizes mouse 11-beta Hydroxysteroid Dehydrogenase 1 (11b-HSD1). No significant sequence homology is seen with 11b-HSD2 or other proteins.
Isotype:IgG
Calc Applications Abbrev:E
Calc Crossreactivity:Mo Rt Sh
Immunogen:A 16aa synthetic peptide mapping near the N-terminus of mouse 11b-HSD1 (KLH coupled). Peptide sequence homology: mouse and rat: 100%; sheep: 87%; human and chicken: 81%; porcine: 75%; rabbit: 68%.