Target：11β-HSD1

Fields：Steroid hormone biosynthesis;Metabolism of xenobiotics by cytochrome P450;Metabolic pathways;Chemical carcinogenesis - DNA adducts

Gene Name：HSD11B1

Protein Name：Corticosteroid 11-beta-dehydrogenase isozyme 1

Human Gene Id：3290

Human Swiss Prot No：P28845

Mouse Gene Id：15483

Mouse Swiss Prot No：P50172

Rat Gene Id：25116

Rat Swiss Prot No：P16232

Immunogen：Synthesized peptide derived from 11β-HSD1 . at AA range: 20-50

Specificity：11β-HSD1 Polyclonal Antibody detects endogenous levels of 11β-HSD1 protein.

Formulation：Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.

Source：Polyclonal, Rabbit,IgG

Dilution：WB 1:500 - 1:2000. IHC: 1:100-1:300. ELISA: 1:10000.. IF 1:50-200

Purification：The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.

Concentration：1 mg/ml

Storage Stability：-15°C to -25°C/1 year(Do not lower than -25°C)

Other Name：HSD11B1;HSD11;HSD11L;Corticosteroid 11-beta-dehydrogenase isozyme 1;11-beta-hydroxysteroid dehydrogenase 1;11-DH;11-beta-HSD1

Observed Band(KD)：35kD

Background：hydroxysteroid 11-beta dehydrogenase 1(HSD11B1) Homo sapiens The protein encoded by this gene is a microsomal enzyme that catalyzes the conversion of the stress hormone cortisol to the inactive metabolite cortisone. In addition, the encoded protein can catalyze the reverse reaction, the conversion of cortisone to cortisol. Too much cortisol can lead to central obesity, and a particular variation in this gene has been associated with obesity and insulin resistance in children. Mutations in this gene and H6PD (hexose-6-phosphate dehydrogenase (glucose 1-dehydrogenase)) are the cause of cortisone reductase deficiency. Alternate splicing results in multiple transcript variants encoding the same protein.[provided by RefSeq, May 2011],

Function：catalytic activity:An 11-beta-hydroxysteroid + NADP(+) = an 11-oxosteroid + NADPH.,disease:Defects in HSD11B1 are a cause of cortisone reductase deficiency (CRD) [MIM:604931]. In CRD, activation of cortisone to cortisol does not occur, resulting in adrenocorticotropin-mediated androgen excess and a phenotype resembling polycystic ovary syndrome (PCOS).,function:Catalyzes reversibly the conversion of cortisol to the inactive metabolite cortisone. Catalyzes reversibly the conversion of 7-ketocholesterol to 7-beta-hydroxycholesterol. In intact cells, the reaction runs only in one direction, from 7-ketocholesterol to 7-beta-hydroxycholesterol.,PTM:Glycosylated.,similarity:Belongs to the short-chain dehydrogenases/reductases (SDR) family.,subunit:Homodimer.,tissue specificity:Widely expressed. Highest expression in liver.,

Subcellular Location：Endoplasmic reticulum membrane ; Single-pass type II membrane protein .

Expression：Widely expressed, highest expression in liver, lower in testis, ovary, lung, foreskin fibroblasts, and much lower in kidney (PubMed:1885595). Expressed in liver (at protein level) (PubMed:21453287). Expressed in the basal cells of the corneal epithelium and in the ciliary nonpigmented epithelium (both at mRNA and at protein level) (PubMed:11481269).