| Detection range: | 0.156-10ng/mL |
| Sensitivity: | 0.048ng/mL |
| Type: | Traditional HSD17β14 ELISA kit |
| Synonyms: | DHRS10; RetSDR3, SDR47C1; Retinal Short-Chain Dehydrogenase/Reductase 3; Short Chain Dehydrogenase/Reductase Family 47C,Member 1 |
| Species: | Human |
| Sample type: | tissue homogenates, cell lysates or other biological fluids. |
| Experimental method: | Sandwich |
| Shelf life: | 12 months |
| Gene ID: | 51171 |
| UniProt ID: | Q9BPX1 |
| Components: | 1. Pre-coated, ready to use 96-well strip plate 1 2. Plate sealer for 96 wells 2 3. Standard 2 4. Diluents buffer: 1×45 mL 5. Detection Reagent A: 1×120 μL 6. Detection Reagent B: 1×120 μL 7. TMB Substrate: 1×9 mL 8. Stop Solution: 1×6 mL 9. Wash Buffer (30× concentrate): 1×20 mL |
Background
There are at least two isozymes of the corticosteroid 11-beta-dehydrogenase, a microsomal enzyme complex responsible for the interconversion of cortisol and cortisone. The type I isozyme has both 11-beta-dehydrogenase (cortisol to cortisone) and 11-oxoreductase (cortisone to cortisol) activities. The type II isozyme, encoded by this gene, has only 11-beta-dehydrogenase activity. In aldosterone-selective epithelial tissues such as the kidney, the type II isozyme catalyzes the glucocorticoid cortisol to the inactive metabolite cortisone, thus preventing illicit activation of the mineralocorticoid receptor. In tissues that do not express the mineralocorticoid receptor, such as the placenta and testis, it protects cells from the growth-inhibiting and/or pro-apoptotic effects of cortisol, particularly during embryonic development. Mutations in this gene cause the syndrome of apparent mineralocorticoid excess and hypertension.
