癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
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 |
| 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 |
For Research Use Only. Not For Use In Diagnostic Procedures.
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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