HSD11B1
HSD11B1 (hydroxysteroid 11-beta dehydrogenase 1, also known as SDR26C1, HSD11B and HSD11) is an NADP(H)-dependent microsomal enzyme of the short-chain dehydrogenase/reductase family. It controls the interconversion of cortisone and cortisol, regulating the local availability of active glucocorticoids. Browse Assay Genie's current range of HSD11B1 research reagents below, or read on for the biology behind the target.
HSD11B1 controls the reversible conversion of biologically active glucocorticoids, turning cortisone into cortisol and 11-dehydrocorticosterone into corticosterone in the presence of NADP(H). The enzyme is bidirectional in vitro but predominantly acts as a reductase in vivo, so it raises the concentration of active glucocorticoids. It takes part in the corticosteroid receptor-mediated anti-inflammatory response and in metabolic and homeostatic processes, and it contributes to aqueous humour secretion in the eye, helping to maintain a normotensive intraocular environment.
Substrate specificity is broad. Besides glucocorticoids, HSD11B1 accepts other steroid and sterol substrates. It interconverts 7-oxo- and 7-hydroxy-neurosteroids such as 7-oxopregnenolone and 7beta-hydroxypregnenolone, and it converts the dietary oxysterol 7-ketocholesterol into the more polar 7-beta-hydroxycholesterol. That oxysterol is linked to apoptosis, accumulation in atherosclerotic lesions, lipid peroxidation and foam cell formation. The enzyme also reduces 7-oxolithocholate, mainly to chenodeoxycholate, which connects glucocorticoid activation with bile acid metabolism. In vitro it forms 7-beta-25-dihydroxycholesterol, a ligand of the GPCR EBI2 that may regulate immune cell migration.
The HSD11B1 gene encodes a 292-residue microsomal protein that sits in the endoplasmic reticulum membrane, and alternate splicing gives multiple transcript variants that encode the same protein. HSD11B1 belongs to the short-chain dehydrogenase/reductase superfamily. Excess 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 in H6PD cause cortisone reductase deficiency. Earlier names include hydroxysteroid (11-beta) dehydrogenase 1.
HSD11B1 interconverts cortisone and cortisol and predominantly acts as a reductase in vivo, making it central to studies of local glucocorticoid activation.
Excess cortisol can lead to central obesity, and a variation in this gene has been associated with obesity and insulin resistance in children.
The enzyme converts 7-ketocholesterol to 7-beta-hydroxycholesterol and reduces 7-oxolithocholate, linking glucocorticoid activation to sterol and bile acid metabolism.
HSD11B1 participates in the corticosteroid receptor-mediated anti-inflammatory response and forms an EBI2 ligand that may regulate immune cell migration.
HSD11B1 controls the reversible conversion of cortisone to cortisol, and of 11-dehydrocorticosterone to corticosterone, using NADP(H). It works in both directions in vitro but mainly acts as a reductase in vivo, increasing active glucocorticoid levels. It also accepts other steroid and sterol substrates.
HGNC lists the full name as hydroxysteroid 11-beta dehydrogenase 1, with the earlier name hydroxysteroid (11-beta) dehydrogenase 1. Aliases and previous symbols include SDR26C1, HSD11B and HSD11. UniProt calls the protein 11-beta-hydroxysteroid dehydrogenase 1 (EC 1.1.1.146).
Mouse and rat both have an ortholog named Hsd11b1; check the datasheet of any product for its validated reactivity. In humans, mutations in HSD11B1 and H6PD cause cortisone reductase deficiency, and a gene variation has been associated with obesity and insulin resistance in children.
Other hydroxysteroid dehydrogenases, steroid-metabolism enzymes and pathway partners of HSD11B1 with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P28845; product specifications from Assay Genie datasheets.