Hydroxysteroid Dehydrogenase, 11-beta, Type I (11b-HSD1)

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.\n\nApplications: \nSuitable for use in ELISA and Western Blot. Other applications not tested.\n\nRecommended Dilution:\nWestern Blot: 1:1000-1:5000 using ECL\nELISA: 1:10,000-1:100,000. Use 50-100ng of control peptide.\nOptimal dilutions to be determined by the researcher.\n\nControl Peptide: H9117-70\n\nStorage and Stability:\nMay be stored at 4 degrees C for short-term only. For long-term storage, store at -20 degrees C. Aliquots are stable for at least 12 months at -20 degrees 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.

Prices direct from United States Biological

Quick response times

Exclusive Biosave savings/discounts

SPECIFICATIONS

Catalog Number

H9117-60

Size

50ul

Applications

ELISA, WB

Hosts

Rabbit

Reactivities

Mouse, Rat, Sheep

Form

Supplied as a liquid in PBS, 0.05% sodium azide, 40% glycerol.

P Type

Pab

Purity

Serum

Isotype

IgG

References

1. Rajan, V., et al. (1995) J. Steroid Biochem. Mol. Biol. 52: 141. 2. Oppermann, U.C., et al. (1995) Eur. J. Biochem. 227: 202. 3. Tannin, G.M., et al. (1991) JBC 266: 166533 4. Agarwal, A.K., et al. (1989) JBC 264: 18939. 5. Masuzaki, et al. (2001) Science 294: 2166. 6. Odermatt, et al. (1999) J. Bio. Chem. 274: 28762. 7. Blum, et al. (2000) BBRC. 276: 428.

Additional Info

Recognizes mouse 11-beta Hydroxysteroid Dehydrogenase 1 (11b-HSD1). No significant sequence homology is seen with 11b-HSD2 or other proteins.