AKR1C1 Antibody
Purified Rabbit Polyclonal Antibody (Pab)
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Application
| WB, IHC-P |
|---|---|
| Primary Accession | Q04828 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 36788 Da |
| Gene ID | 1645 |
|---|---|
| Other Names | Aldo-keto reductase family 1 member C1, 111-, 20-alpha-hydroxysteroid dehydrogenase, 20-alpha-HSD, Chlordecone reductase homolog HAKRC, Dihydrodiol dehydrogenase 1/2, DD1/DD2, High-affinity hepatic bile acid-binding protein, HBAB, Indanol dehydrogenase, Trans-1, 2-dihydrobenzene-1, 2-diol dehydrogenase, AKR1C1, DDH, DDH1 |
| Dilution | WB~~1:1000 IHC-P~~1:50~200 |
| Format | 0.01M PBS, pH 7.2, 0.09% (W/V) Sodium azide, Glycerol 50% |
| Storage | Store at -20 °C.Stable for 12 months from date of receipt |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | AKR1C1 |
|---|---|
| Synonyms | DDH, DDH1 |
| Function | Cytosolic aldo-keto reductase that catalyzes NADPH-dependent reduction of ketosteroids to hydroxysteroids. Displays broad substrate specificity with distinct positional and stereochemistry, primarily generating 20alpha-hydroxysteroids, but also 3alpha/beta- and 17beta- hydroxysteroids (PubMed:10998348, PubMed:11013348, PubMed:14672942, PubMed:19218247, PubMed:11995921, PubMed:12604236). Involved in neurosteroid metabolism. Reduces 5alpha-dihydrodeoxycorticosterone (5- alpha-DHDOC) to neuroactive steroid 3alpha,5alpha- tetrahydrodeoxycorticosterone (3alpha,5alpha-THDOC) known to alter neural excitability via allosteric activation of gamma-aminobutyric acid type A (GABAAR) receptors. Inactivates 3alpha-hydroxy-5alpha- pregnan-20-one (3alpha,5alpha-THP) into less potent neurosteroid 3alpha,20alpha-dihydroxy-5alpha-pregnane (PubMed:11995921, PubMed:12604236). Catalyzes the reduction of progesterone to less potent progestogen (20S)-hydroxypregn-4-en-3-one likely regulating ligand availability for progesterone receptors (PubMed:10998348, PubMed:11013348, PubMed:12604236). In androgen catabolism, may predominantly act as a phase I enzyme by introducing a hydroxyl group prior to conjugation. It can nevertheless participate in the alternative phase II pathway by directly reducing sulfate- or glucuronide-conjugated androgens (PubMed:19218247). In vitro can efficiently catalyze bidirectional conversion between ketosteroids and hydroxysteroids using NADPH/NADP(+) or NADH/NAD(+) as cofactors. In vivo however, the reductase activity prevails since the major reducing cofactor NADPH inhibits NAD(+)-dependent oxidase activity (PubMed:14672942). |
| Cellular Location | Cytoplasm, cytosol. |
| Tissue Location | Expressed in all tissues tested including liver, prostate, testis, adrenal gland, brain, uterus, mammary gland and keratinocytes. Highest levels found in liver, mammary gland and brain |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Converts progesterone to its inactive form, 20-alpha- dihydroxyprogesterone (20-alpha-OHP). In the liver and intestine, may have a role in the transport of bile. May have a role in monitoring the intrahepatic bile acid concentration. Has a low bile-binding ability. May play a role in myelin formation.
REFERENCES
Stolz A.,et al.J. Biol. Chem. 268:10448-10457(1993).
Lou H.,et al.J. Biol. Chem. 269:8416-8422(1994).
Ciaccio P.J.,et al.J. Biol. Chem. 269:15558-15562(1994).
Khanna M.,et al.J. Steroid Biochem. Mol. Biol. 53:41-46(1995).
Nishizawa M.,et al.Genes Cells 5:111-125(2000).
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