HSD11B2 Knockout cell line (HEK293)
Catalog Number: KO37190
Price: Online Inquiry
Catalog Number: KO37190
Price: Online Inquiry
Product Information | |
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Product Name | HSD11B2 Knockout cell line (HEK293) |
specification | 1*10^6 |
Storage and transportation | Dry ice preservation/T25 live cell transportation. |
Cell morphology | Epithelioid, adherent cell |
Passage ratio | 1:3~1:6 |
species | Human |
Gene | HSD11B2 |
Gene ID | 3291 |
Build method | Electric rotation method / virus method |
Mycoplasma testing | Negative |
Cultivation system | 90%DMEM+10% FBS |
Parental Cell Line | HEK293 |
Quality Control | Genotype: HSD11B2 Knockout cell line (HEK293) >95% viability before freezing. All cells were tested and found to be free of bacterial, viruses,mycoplasma and other toxins. |
Gene Information | |
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Gene Official Full Name | hydroxysteroid 11-beta dehydrogenase 2provided by HGNC |
Also known as | AME; AME1; HSD2; HSD11K; SDR9C3 |
Gene Description | 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. [provided by RefSeq, Feb 2010] |
Expression | Biased expression in kidney (RPKM 155.7), colon (RPKM 97.2) and 6 other tissues See more |
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