Technical Data
A1334-70Y
AKR1C4, Recombinant, Human, His-Tag (Aldo-keto Reductase Family 1 Member C4, 3-alpha-HSD1, 3-alpha-hydroxysteroid Dehydrogenase Type I, Chlordecone Reductase, CDR, Dihydrodiol Dehydrogenase 4, DD-4, DD4, HAKRA, CHDR)
20ug
Molecular Biology Storage: -20CShipping: Blue Ice
Aldo-keto Reductase 1C4 (AKR1C4), also known as dihydrodiol dehydrogenase 4, is a member of the aldo-keto reductase (AKR) superfamily. It catalyzes the reversible oxidoreduction of various 3a-hydroxysteroids and prostaglandins as well as the oxidation of trans-dihydrodiols of aromatic hydrocarbons and alicyclic alcohols. AKR1C4 is important for steroid hormone metabolism primarily through synthesis and clearance of testosterone. Its high expression in liver and the ability to reduce xenobiotic carbonyl compounds suggests an important role in xenobiotic metabolism, as is manifested by the detoxification of the pesticide chlordecone in humans. AKR1C4 also plays a role in the pharmacokinetics of various drugs and prodrug activation.

Source:
Recombinant corresponding to aa1-323 from human AKR1C4, expressed in E. coli.

Molecular Weight:
~37kD

Biological Activity:
Measured by its NADP+-dependent oxidation of cholic acid.

Specific Activity:
>300pmol/min/ug

Endotoxin: ~1EU/1ug (LAL)

Storage and Stability:
May be stored at 4C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20C. Aliquots are stable for at least 12 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Molecular Weight:
~37kD
Source: E. coli
Purity: ~90% (SDS-PAGE)
Concentration: As reported
Form: Supplied as a liquid in Tris, sodium chloride, DTT, glycerol. BSA free.

Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications without the expressed written authorization of United States Biological.
1. Penning, P. M. et al. (1990) Steroids 47:221. 2. Takikawa, H. et al. (1992) Hepatology 16:365. 3. Binstock, J. M. et al. (1992) Biochem. Biophys. Res. Commun. 187:760. 4. Ohara, H. et al. (1994) Biochim. Biophys. Acta. 1215:59. 5. Winters, C. J. et al. (1990) Biochemistry 29:1080. 6. Jin, Y. et al. (2009) J. Biol. Chem. 284:10013. 7. Breyer-Pfaff, U. et al. (2004) J. Pharm. Pharmacol. 56:1601.

Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.