Description
Product Usage Information
Western Blotting: 1:1000
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at -20°C. Do not aliquot the antibody.
Protocol
Available protocols: Western Blotting
Specificity / Sensitivity
AKR1C2 Antibody recognizes endogenous levels of total AKR1C2 protein.
Species Reactivity: Human, Mouse, Rat
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val61 of human AKR1C2 protein. Antibodies are purified by protein A and peptide affinity chromatography.
Background
Aldo-keto reductase family 1 member C2 (AKR1C2) is a member of a large superfamily of aldo-keto reductases that metabolize an array of substrates in a NADPH-dependent manner. AKR1C2 is the 3-α-hydroxysteroid dehydrogenase (3α-HSD) responsible for metabolizing and inactivating the androgen hormone 5α-dihydrotestosterone (DHT) to 3α-androstanediol (1). Research studies demonstrate an increase in AKR1C2 expression in cases of advanced prostate cancer (2). Both AKR1C2 and the related reductase, AKR1C3, are implicated in enhancing PI3K/Akt signaling in prostate cancer by reducing prostaglandin D2 to the more stable 9α, 11β-PGF2α (2). In addition, research studies demonstrate an increase in AKR1C2 expression in some ovarian endometriosis specimens, suggesting the participation of AKR1C2 in the promotion of progesterone metabolism in ovarian endometriosis (3).
Alternate Names
3-alpha hydroxysteroid dehydrogenase, type III; 3-alpha hydroxysteroid dehydrogenase, type III); 3-alpha-HSD3; AK1C2; AKR1C-pseudo; AKR1C2; Aldo-keto reductase family 1 member C2; aldo-keto reductase family 1, member C2 (dihydrodiol dehydrogenase 2; BABP; bile acid binding protein; Chlordecone reductase homolog HAKRD; DD; DD-2; DD/BABP; DD2; DDH2; Dihydrodiol dehydrogenase 2; Dihydrodiol dehydrogenase/bile acid-binding protein; FLJ53800; HAKRD; HBAB; MCDR2; pseudo-chlordecone reductase; SRXY8; TDD; testicular 17,20-desmolase deficiency; Trans-1,2-dihydrobenzene-1,2-diol dehydrogenase; type II dihydrodiol dehydrogenase; Type III 3-alpha-hydroxysteroid dehydrogenase
