protein

AKR1D1, 1-326aa, Human, His tag, E Coli

MBS203963

0.1 mg

310 USD

Recombinant Protein

AKR1D1, 1-326aa, Human, His tag, E Coli

AKR1D1

Aldo-keto reductase family 1; member D1; 3o5bred; CBAS2; SRD5B1

3-oxo-5-beta-steroid 4-dehydrogenase isoform 1; 3-oxo-5-beta-steroid 4-dehydrogenase; 3-oxo-5-beta-steroid 4-dehydrogenase; delta 4-3-ketosteroid-5-beta-reductase; delta(4)-3-ketosteroid 5-beta-reductase; delta(4)-3-oxosteroid 5-beta-reductase; steroid-5-beta-reductase, beta polypeptide 1 (3-oxo-5 beta-steroid delta 4-dehydrogenase beta 1); aldo-keto reductase family 1, member D1; Aldo-keto reductase family 1 member D1; Delta(4)-3-ketosteroid 5-beta-reductase; Delta(4)-3-oxosteroid 5-beta-reductase

AKR1D1

AKR1D1; AKR1D1; CBAS2; SRD5B1; 3o5bred; SRD5B1

AK1D1_HUMAN

326

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

> 90% by SDS - PAGE

Liquid. In 20mM Tris-HCl buffer (pH 8.0) containing 1mM DTT, 20% glycerol, 100mM NaCl

0.5 mg/ml (determined by Bradford assay)

Can be stored at 4 degree C short term (1-2 weeks). For long term storage, aliquot and store at -20 degree C or -70 degree C. Avoid repeated freezing and thawing cycles.

SDS-PAGE

Antigen Species: Human. Tag: His-tag

Expression System: E Coli. Bioactivity: Specific activity: > 1.0 units/mg (Please enquire for specific batch value). Enzymatic activity was confirmed by measuring the amount of enzyme catalyzing the oxidation of 1 micromole NADPH/min at 25C. Assay: 1. Prepare a 1 ml reaction mix into a suitable container: . The final concentrations are 0.1M sodium phosphate (pH7.0), 10mM DL-glyceraldehyde, 0.3mM NADPH. 2. Add 50ul of recombinant AKR1D1 protein solution with various concentrations (1ug, 2ug) in 750ul reaction buffer. 3. Mix by inversion and incubate at 25C for 2.5 minutes. 4. Add 200ul of 50 mM DL-glyceraldehyde as a substrate and immediately mix by inversion. 5. Record the decrease in A340nm for 3 minutes.

Metabolism

Aldo-keto reductase family 1, member D1, also known as AKR1D1, is a member of the AKR superfamily. The AKR family of proteins are 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.

Charbonneau A., et al. (2001) Biochim Biophys Acta. 1517:228-235. Lemonde H A., et al. (2003) Gut. 52:1494-1499.

5174695

NP_005980

NM_005989.3

39.5 kDa (346aa) confirmed by MALDI-TOF

Bile Acid And Bile Salt Metabolism Pathway (106144); Bile Acid Biosynthesis, Cholesterol = Cholate/chenodeoxycholate Pathway (413432); Bile Acid Biosynthesis, Cholesterol = Cholate/chenodeoxycholate Pathway (468297); Metabolic Pathways (132956); Metabolism Pathway (477135); Metabolism Of Lipids And Lipoproteins Pathway (160976); Primary Bile Acid Biosynthesis Pathway (82938); Primary Bile Acid Biosynthesis Pathway (299); Steroid Hormone Biosynthesis Pathway (82940); Steroid Hormone Biosynthesis Pathway (301)

The enzyme encoded by this gene is responsible for the catalysis of the 5-beta-reduction of bile acid intermediates and steroid hormones carrying a delta(4)-3-one structure. Deficiency of this enzyme may contribute to hepatic dysfunction. Three transcript variants encoding different isoforms have been found for this gene. Other variants may be present, but their full-length natures have not been determined yet. [provided by RefSeq, Jul 2010]

AKR1D1: Efficiently catalyzes the reduction of progesterone, androstenedione, 17-alpha-hydroxyprogesterone and testosterone to 5-beta-reduced metabolites. The bile acid intermediates 7- alpha,12-alpha-dihydroxy-4-cholesten-3-one and 7-alpha-hydroxy-4- cholesten-3-one can also act as substrates. Defects in AKR1D1 are the cause of congenital bile acid synthesis defect type 2 (CBAS2); also known as cholestasis with delta(4)-3-oxosteroid 5-beta-reductase deficiency. Patients with this liver disease show absence or low levels of chenodeoxycholic acid and cholic acid in plasma and urine. Belongs to the aldo/keto reductase family. 3 isoforms of the human protein are produced by alternative splicing. Protein type: EC 1.3.1.3; Lipid Metabolism - androgen and estrogen; Oxidoreductase; Lipid Metabolism - primary bile acid biosynthesis; Lipid Metabolism - C21-steroid hormone. Chromosomal Location of Human Ortholog: 7q32-q33. Cellular Component: cytosol. Molecular Function: delta4-3-oxosteroid 5beta-reductase activity; steroid binding. Biological Process: bile acid biosynthetic process; bile acid metabolic process; bile acid catabolic process; C21-steroid hormone metabolic process; digestion; androgen metabolic process; cholesterol catabolic process. Disease: Bile Acid Synthesis Defect, Congenital, 2

0.1 mg

310 USD

0.5 mg

720