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Anti-Human AKR1C3 Polyclonal Antibody (HW642014)

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Overview
Catalog No.HW642014
Species reactivityHuman
ApplicationsELISA, IHC, WB
Host speciesRabbit
ClonalityPolyclonal
IsotypeIgG
Immunogen E. coli - derived recombinant Human AKR1C3 (Met1-Tyr323).
Target 3-alpha-hydroxysteroid dehydrogenase type 2, Aldo-keto reductase family 1 member C3, Testosterone 17-beta-dehydrogenase 5, 3-alpha-HSD type II, brain, DD3, DD-3, PGFS, Prostaglandin F synthase, 17-beta-HSD 5, Chlordecone reductase homolog HAKRb, Dihydrodiol dehydrogenase type I, Dihydrodiol dehydrogenase 3, HSD17B5, 17-beta-hydroxysteroid dehydrogenase type 5, HA1753, KIAA0119, DDH1, 3-alpha-HSD type 2, AKR1C3
Purification Purified by antigen affinity column.
Accession P42330
Form Liquid
Storage buffer 0.01M PBS, pH 7.4, 50% Glycerol, 0.05% Proclin 300.

Please refer to the specific buffer information in the hardcopy of datasheet or the lot-specific COA.

Product Usage Information
Application Dilution
ELISA 1:5000-1:20000
IHC 1:50-1:500
WB 1:500-1:2000
Stability and Storage Use a manual defrost freezer and avoid repeated freeze thaw cycles. Store at 2 to 8°C for frequent use. Store at -20 to -80°C for twelve months from the date of receipt.
Background

Aldo-keto reductase family 1 member C3 (AKR1C3) is a ~36 kDa protein. Cytosolic aldo-keto reductase that catalyzes NADPH-dependent reduction of ketosteroids to hydroxysteroids. Displays broad substrate specificity with distinct positional and stereochemistry, primarily generating 17beta-hydroxysteroids, but also 3alpha- and 20alpha-hydroxysteroids. Produces potent androgens via classical and 'backdoor'/alternative pathways. In the classical androgen metabolic pathway (biosynthesis of 5alpha-dihydrotestosterone (5alpha-DHT) via testosterone), catalyzes the reduction of delta4-androstenedione to form testosterone. In the 'backdoor' androgen metabolic pathway (biosynthesis of 5alpha-dihydrotestosterone (5alpha-DHT) via pregnanes), reduces androsterone to 5alpha-androstane-3alpha,17beta-diol preceding 5alpha-DHT secretion.

1. Penning, TM. et al. (2000) The Biochemical journal 351, 67-77. PMID: 10998348
2. Penning, TM. et al. (2001) Molecular and cellular endocrinology 171, 137-49. PMID: 11165022
3. Byrns, MC. et al. (2010) The Journal of steroid biochemistry and molecular biology 118, 177-87. PMID: 20036328
4. Lin, HK. et al. (1997) Molecular endocrinology (Baltimore, Md.) 11, 1971-84. PMID: 9415401
5. Dufort, I. et al. (1999) Endocrinology 140, 568-74. PMID: 9927279
7. Steckelbroeck, S. et al. (2004) The Journal of biological chemistry 279, 10784-95. PMID: 14672942
8. Khanna, M. et al. (1995) The Journal of biological chemistry 270, 20162-8. PMID: 7650035
9. Endo, S. et al. (2020) The Journal of steroid biochemistry and molecular biology 199, 105586. PMID: 31926269
Note For research use only.
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Formula
Mass (g) = Concentration (mol/L) × Volume (L) × MW (g/mol)
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Formula
C₁ × V₁ = C₂ × V₂
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Stock Solution
C₁ (Stock Conc.)
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V₁ (Stock Vol.)
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Working Solution
C₂ (Working Conc.)
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