3-Oxo-5-Beta-Steroid 4-Dehydrogenase (AKR1D1) Antibody

Este producto es parte de AKR1D- Aldo-keto reductase family 1 member D
3-Oxo-5-Beta-Steroid 4-Dehydrogenase (AKR1D1) Antibody
377€ (100 µg)

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Name
3-Oxo-5-Beta-Steroid 4-Dehydrogenase (AKR1D1) Antibody
Category
Primary Antibodies
Provider
Abbexa
Reference
abx230265
Tested Applications
ELISA, WB

Description

AKR1D1 Antibody is a Rabbit Polyclonal against AKR1D1.

Documentos del producto

Instrucciones
Data sheet
Descargar

Especificaciones del producto

Category
Primary Antibodies
Immunogen Target
Target: 3-Oxo-5-Beta-Steroid 4-Dehydrogenase (AKR1D1)
Immunogen: aldo-keto reductase family 1, member D1 (delta 4-3-ketosteroid-5-beta-reductase)
Host
Rabbit
Reactivity
Human, Mouse, Rat
Assay Type
Concentration: 2 mg/ml
Recommended Dilution
WB: 1/200 - 1/2000. Optimal dilutions/concentrations should be determined by the end user.
Clonality
Polyclonal
Conjugation
Unconjugated
Isotype
IgG
Observed MW
Observed MW: 37 kDa
Purity
≥ 95% (SDS-PAGE)
Purification
Purified by immunogen affinity chromatography.
Size 1
100 µg
Form
Liquid
Tested Applications
ELISA, WB
Buffer
PBS, pH 7.3, with 0.02% sodium azide and 50% glycerol.
Availability
Shipped within 5-12 working days.
Storage
Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
P51857
Gene ID
6718
OMIM
235555
Alias
AKR1D1,SRD5B1
Background
Antibody anti-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.

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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