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AKR1D1, human recombinant protein
Aldo-keto reductase family 1, member D1, 3o5bred, CBAS2, SRD5B1
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | P51857 |
|---|---|
| Concentration | 0.5 |
| Calculated MW | 39.5 kDa (346 aa, 1-326 aa + His Tag), confirmed by MALDI-TOF. |
| Gene ID | 6718 |
|---|---|
| Gene Symbol | AKR1D1 |
| Other Names | Aldo-keto reductase family 1, member D1, 3o5bred, CBAS2, SRD5B1 |
| Gene Source | Human |
| Source | E. coli |
| Assay&Purity | SDS-PAGE; ≥90% |
| Assay2&Purity2 | N/A; |
| Recombinant | Yes |
| Sequence | MGSSHHHHHH SSGLVPRGSH MDLSAASHRI PLSDGNSIPI IGLGTYSEPK STPKGACATS VKVAIDTGYR HIDGAYIYQN EHEVGEAIRE KIAEGKVRRE DIFYCGKLWA TNHVPEMVRP TLERTLRVLQ LDYVDLYIIE VPMAFKPGDE IYPRDENGKW LYHKSNLCAT WEAMEACKDA GLVKSLGVSN FNRRQLELIL NKPGLKHKPV SNQVECHPYF TQPKLLKFCQ QHDIVITAYS PLGTSRNPIW VNVSSPPLLK DALLNSLGKR YNKTAAQIVL RFNIQRGVVV IPKSFNLERI KENFQIFDFS LTEEEMKDIE ALNKNVRFVE LLMWRDHPEY PFHDEY |
| Target/Specificity | AKR1D1 |
| Format | Liquid |
| Storage | -80°C; 0.5 mg/ml in 20 mM Tris-HCl buffer (pH 8.0) containing 1 mM DTT, 100 mM NaCl and 20% glycerol. |
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Background
Aldo-keto reductase family 1, member D1, also known as AKR1D1, is a member of the AKR superfamily. The AKR family of proteins is soluble NADPH oxidoreductases. They play important roles in the metabolism of drugs, carcinogens and reactive aldehydes. AKR1D1 is responsible for the catalysis of the 5-beta-reduction of bile acid intermediates and steroid hormones which carry a delta (4)-3-one structure. AKR1D1 is highly expressed in liver, colon and testis. Deficiency of this enzyme may contribute to hepatic dysfunction. Recombinant human AKR1D1 protein, fused to His-tag at N-terminus, was expressed in E.coli and purified by using conventional chromatography techniques.
References
Kondo K.-H.,et al.Eur. J. Biochem. 219:357-363(1994).
Charbonneau A.,et al.Biochim. Biophys. Acta 1517:228-235(2001).
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Hillier L.W.,et al.Nature 424:157-164(2003).
Scherer S.W.,et al.Science 300:767-772(2003).
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