Recombinant Human HSD11B2, GST-tagged
Cat.No. : | HSD11B2-13953H |
Product Overview : | Recombinant Human HSD11B2 (1 a.a. - 405 a.a.), fused with GST-tag at N-terminal, was expressed in wheat germ. |
- Specification
- Gene Information
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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. |
Source : | Wheat germ |
Species : | Human |
Tag : | GST |
Molecular Mass : | 70.5 kDa |
AA Sequence : | MERWPWPSGGAWLLVAARALLQLLR SDLRLGRPLLAALALLAALDWLCQR LLPPPAALAVLAAAGWIALSRLARP QRLPVATRAVLITGCDSGFGKETAK KLDSMGFTVLATVLELNSPGAIELR TCCSPRLRLLQMDLTKPGDISRVLE FTKAHTTSTGLWGLVNNAGHNEVVA DAELSPVATFRSCMEVNFFGALELT KGLLPLLRSSRGRIVTVGSPAGDMP YPCLGAYGTSKAAVALLMDTFSCEL LPWGVKVSIIQPGCFKTESVRNVGQ WEKRKQLLLANLPQELLQAYGKDYI EHLHGQFLHSLRLAMSDLTPVVDAI TDALLAARPRRRYYPGQGLGLMYFT HYYLPEGLRRRFLQAFFISHCLPRA LQPGQPGTTPPQDAAQDPNLSPGPS PAVAR |
Applications : | ELISA; WB-Re; AP; Array |
Notes : | Best use within three months from the date of receipt of this protein. |
Storage : | Store at -80°C. Aliquot to avoid repeated freezing and thawing. |
Storage Buffer : | 50 mM Tris-HCI, 10 mM reduced Glutathione, pH=8.0 in the elution buffer. |
Gene Name : | HSD11B2 hydroxysteroid (11-beta) dehydrogenase 2 [ Homo sapiens (human) ] |
Official Symbol : | HSD11B2 |
Synonyms : | HSD11B2; AME; AME1; HSD2; HSD11K; SDR9C3; hydroxysteroid (11-beta) dehydrogenase 2; corticosteroid 11-beta-dehydrogenase isozyme 2; 11-DH2; 11-beta-HSD2; -HSD11 type II; 11-beta-hydroxysteroid dehydrogenase type 2; 11-beta-hydroxysteroid dehydrogenase type II; NAD-dependent 11-beta-hydroxysteroid dehydrogenase; short chain dehydrogenase/reductase family 9C member 3; NP_000187.3; EC 1.1.1.146 |
Gene ID : | 3291 |
mRNA Refseq : | NM_000196 |
Protein Refseq : | NP_000187 |
MIM : | 614232 |
UniProt ID : | P80365 |
Chromosome Location : | 16q22 |
Pathway : | Aldosterone-regulated sodium reabsorption; C21-Steroid hormone biosynthesis, progesterone => cortisol/cortisone; Glucocorticoid & Mineralcorticoid Metabolism |
Function : | 11-beta-hydroxysteroid dehydrogenase [NAD(P)] activity; NAD binding; steroid binding |
Products Types
◆ Recombinant Protein | ||
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HSD11B2-4331M | Recombinant Mouse HSD11B2 Protein, His (Fc)-Avi-tagged | +Inquiry |
Hsd11b2-1176M | Recombinant Mouse Hsd11b2 Protein, MYC/DDK-tagged | +Inquiry |
HSD11B2-1416H | Recombinant Human HSD11B2 Protein (1-405 aa), His-tagged | +Inquiry |
◆ Lysates | ||
HSD11B2-5378HCL | Recombinant Human HSD11B2 293 Cell Lysate | +Inquiry |
Related Gene
For Research Use Only. Not intended for any clinical use. No products from Creative BioMart may be resold, modified for resale or used to manufacture commercial products without prior written approval from Creative BioMart.
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Q&As (7)
Ask a questionThe expression of HSD11B2 is regulated by various factors in different tissues. In the kidney, where HSD11B2 plays a crucial role in glucocorticoid metabolism, its expression is primarily regulated by aldosterone through the activation of mineralocorticoid receptors. Additionally, other factors, such as angiotensin II and pro-inflammatory cytokines, can also modulate HSD11B2 expression. In tissues outside the kidney, including adipose tissue and the central nervous system, HSD11B2 expression is regulated by a combination of hormonal, metabolic, and inflammatory signals.
Altered HSD11B2 activity has been implicated in various metabolic diseases. For instance, decreased HSD11B2 activity in adipose tissue has been associated with increased local cortisol levels, contributing to the development of obesity, insulin resistance, and metabolic syndrome. Conversely, increased HSD11B2 activity in other tissues, such as the liver, has been associated with reduced cortisol availability, which may impact glucose metabolism and contribute to the development of hepatic insulin resistance. Understanding the precise mechanisms underlying these associations is crucial for developing targeted therapeutic strategies.
HSD11B2 plays a crucial role in cardiovascular health by regulating the balance between cortisol and aldosterone action. Dysregulation of this balance, due to altered HSD11B2 activity, can contribute to the development and progression of cardiovascular diseases. For example, increased cortisol activation of mineralocorticoid receptors in the vasculature can lead to endothelial dysfunction, vascular inflammation, and hypertension. Furthermore, altered HSD11B2 expression in the heart and blood vessels has been associated with cardiac remodeling, fibrosis, and impaired contractility. Understanding the precise mechanisms underlying these effects can provide insights into potential therapeutic interventions.
Several potential therapeutic strategies targeting HSD11B2 have been explored. These include the development of selective inhibitors that can block the enzyme's activity, leading to increased cortisol availability in specific tissues. Conversely, activators of HSD11B2 could enhance its protective role by promoting cortisol inactivation. Additionally, modulating HSD11B2 expression and activity through lifestyle interventions, such as diet and exercise, may also have therapeutic potential. However, further research is needed to evaluate the efficacy and safety of these strategies in clinical settings.
The role of HSD11B2 in stress and mental health is an area of active research. Chronic stress has been associated with dysregulation of the hypothalamic-pituitary-adrenal axis and increased cortisol levels, which can influence HSD11B2 activity. Altered HSD11B2 expression and activity in the brain have been implicated in stress-related psychiatric disorders, including depression and anxiety. Furthermore, studies have suggested a potential link between HSD11B2 polymorphisms and susceptibility to stress-related mental health conditions. However, more research is needed to fully elucidate the complex interplay between HSD11B2, cortisol metabolism, and mental health outcomes.
Yes, genetic variations in HSD11B2 have been reported to be associated with disease susceptibility. Single nucleotide polymorphisms (SNPs) in the HSD11B2 gene have been linked to altered enzyme activity and increased risk of developing conditions such as hypertension, cardiovascular disease, and metabolic disorders. These genetic variations can affect HSD11B2 expression, protein stability, or catalytic efficiency, thereby influencing glucocorticoid metabolism and potentially contributing to disease pathogenesis.
HSD11B2, also known as 11β-hydroxysteroid dehydrogenase type 2, plays a critical role in the regulation of glucocorticoid levels. It acts as a protective enzyme by converting active cortisol into inactive cortisone in mineralocorticoid target tissues, such as the kidney. This enzyme prevents cortisol from binding to the mineralocorticoid receptor, thereby maintaining the selective action of aldosterone on mineralocorticoid receptors. Dysfunction or deficiency of HSD11B2 can lead to excessive cortisol activation of mineralocorticoid receptors, resulting in conditions such as apparent mineralocorticoid excess syndrome.
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