Control peptide for H9117-60(antiserum) and H9117-65 (affintity purified antibody).
Synthetic peptide corresponding to 16aa of mouse 11b-HSD1 conjugated to KLH.
Species Sequence Homology:100% conserved in the mouse and rat, 87% in sheep and 81% in human and chicken, 75% in porcine and 68% in rabbit 11b-HSD1. No significant sequence homology is seen with other proteins.
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, Antibody Blocking. Not suitable for use in Western Blot. Other applications not tested.
Recommended Dilutions:ELISA: 50-100ng/wellAntibody Blocking: 5-10ug control peptide per 1ul H9117-60(antiserum)or per 1ug H9117-65 (affintity purified antibody)
Optimal dilutions to be determined by the researcher.
Storage and Stability:May be stored at 4°C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20°C. Aliquots are stable for 6 months after receipt 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.
