Human 3-Oxo-5-Beta-Steroid 4-Dehydrogenase (AKR1D1) Protein
234€ (5 µg)
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Name
Human 3-Oxo-5-Beta-Steroid 4-Dehydrogenase (AKR1D1) Protein
Category
Proteins and Peptides
Provider
Abbexa
Reference
abx073203
Tested Applications
SDS-PAGE
Description
Aldo-Keto Reductase Family 1 Member D1 is a recombinant enzyme.
Documentos del producto
Instrucciones
Data sheet
Especificaciones del producto
| Category | Proteins and Peptides |
| Immunogen Target | 3-Oxo-5-Beta-Steroid 4-Dehydrogenase (AKR1D1) |
| Host | E. coli |
| Assay Type | Activity: Not tested Sequence Fragment: 1-326 AA. Tag: N-terminal His tag |
| Recommended Dilution | Optimal dilutions/concentrations should be determined by the end user. |
| Origin | Human |
| Observed MW | 39.5 kDa |
| Expression | Recombinant |
| Purity | > 90% (SDS-PAGE) |
| Purification | Purified by proprietary chromatographic techniques. |
| Size 1 | 5 µg |
| Size 2 | 20 µg |
| Size 3 | 1 mg |
| Form | Liquid |
| Tested Applications | SDS-PAGE |
| Buffer | 20 mM Tris-HCl buffer (pH 8.0), 1 mM DTT, 20% glycerol and 100 mM NaCl. |
| Availability | Shipped within 5-10 working days. |
| Storage | Store at 4°C if entire vial will be used within 4 weeks. For long-term storage, aliquot and store at -20 °C. For long-term storage, it is recommended to add a carrier protein (0.1% HSA or BSA). Avoid multiple freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | P51857 |
| Gene ID | 6718 |
| Alias | AKR1D1,SRD5B1 |
| Background | Protein AKR1D1 |
| Status | RUO |
| Note | THIS PRODUCT IS FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC, THERAPEUTIC OR COSMETIC PROCEDURES. NOT FOR HUMAN OR ANIMAL CONSUMPTION. Concentration: 0.5 mg/ml |
Background
AKR1D1, also known as Δ4-3-ketosteroid-5β-reductase, is a liver-specific enzyme that plays a pivotal role in bile acid synthesis and steroid hormone metabolism. It catalyzes the reduction of double bonds in Δ4-3-ketosteroids, converting cortisol, aldosterone, and other steroid precursors into their inactive 5β-reduced metabolites. This activity is essential for bile acid production, as AKR1D1 mediates the transformation of cholesterol-derived intermediates into bile acids, which are critical for lipid digestion and cholesterol homeostasis. AKR1D1 deficiency results in bile acid synthesis disorders, leading to cholestasis, liver dysfunction, and fat malabsorption. Additionally, AKR1D1 contributes to steroid clearance and inactivates glucocorticoids, regulating cortisol levels and preventing glucocorticoid excess. Dysregulation of AKR1D1 is linked to liver diseases, such as non-alcoholic fatty liver disease (NAFLD) and cirrhosis, where impaired bile acid synthesis disrupts lipid metabolism. It is also implicated in metabolic syndrome and hormone-driven disorders due to its role in steroid hormone regulation.
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