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。
DD2 Polyclonal Antibody
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Application 
| WB, IHC-P, IF, ICC, E |
|---|---|
| Primary Accession | P52895 |
| Reactivity | Human, Rat, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 36735 Da |
| Gene ID | 1646 |
|---|---|
| Other Names | AKR1C2; DDH2; Aldo-keto reductase family 1 member C2; 3-alpha-HSD3; Chlordecone reductase homolog HAKRD; Dihydrodiol dehydrogenase 2; DD-2; DD2; Dihydrodiol dehydrogenase/bile acid-binding protein; DD/BABP; Trans-1; 2-dihydrobenzene-1, 2-diol |
| Dilution | WB~~Western Blot: 1/500 - 1/2000. Immunohistochemistry: 1/100 - 1/300. ELISA: 1/20000. Not yet tested in other applications. IHC-P~~1:50~200 IF~~1:50~200 ICC~~N/A E~~N/A |
| Format | Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.09% (W/V) sodium azide. |
| Storage Conditions | -20℃ |
| Name | AKR1C2 {ECO:0000303|PubMed:9716498} |
|---|---|
| Synonyms | DDH2 |
| 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 3alpha-hydroxysteroids, but also 3beta-, 17beta- and 20alpha-hydroxysteroids (PubMed:8920937, PubMed:9716498, PubMed:10998348, PubMed:12416991, PubMed:11995921, PubMed:12604236, PubMed:14672942, PubMed:19218247, PubMed:21802064, PubMed:11514561, PubMed:15929998, PubMed:17034817, PubMed:17442338, PubMed:24434280). Required for male sex determination as a component of the 'backdoor' androgen biosynthesis pathway that generates 5alpha-dihydrotestosterone (5alpha-DHT) via pregnanes. Acts together with AKR1C4 to convert 5alpha-dihydroprogesterone (5alpha-DHP) to 3alpha-hydroxy-5alpha- pregnan-20-one (3alpha,5alpha-THP/allopregnanolone), leading to 5alpha- DHT secretion necessary for embryonic gonad differentiation into testis (PubMed:12416991, PubMed:21802064). 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:10998348, PubMed:11514561, PubMed:14672942, PubMed:15929998, PubMed:19218247, PubMed:24434280). In neurosteroid biosynthesis, may preferentially reduce 5alpha- dihydroprogesterone (5-alpha-DHP) and 5alpha-dihydrodeoxycorticosterone (5-alpha-DHDOC) precursors to 3alpha-hydroxy-5alpha-pregnan-20-one (3alpha,5alpha-THP/allopregnanolone) and 3alpha,21-dihydroxy-5alpha- pregnane-20-one (3alpha,5alpha-THDOC) neuroactive steroids known to alter neural excitability via allosteric activation of gamma- aminobutyric acid type A receptors (GABAAR) (PubMed:11995921, PubMed:12416991, PubMed:12604236). Regulates ligand availability for steroid hormone receptors. Catalyzes the inactivation of 5alpha-DHT and progesterone converting them into 3alpha/beta-androstanediols and (20S)-hydroxypregn-4-en-3-one, respectively (PubMed:10998348, PubMed:24434280). Can form 17beta-hydroxysteroids such as testosterone and estradiol albeit with lower efficiency when compared to AKR1C3 (PubMed:10998348). May contribute to the metabolism of adrenal-derived androgens via reduction of 11-keto-5alpha-androstane-3,17-dione (11K- Adione) into 11-ketoandrosterone (11KAST) and of 11- ketodihydrotestosterone (11KDHT) into 11-keto-5alpha-androstane- 3alpha/beta,17beta-diol (11K-A3alphadiol) (PubMed:31926269). May also play a role in prostaglandin (PG) metabolism by reducing PGD2 to 11beta-PGF2 (PubMed:9716498). Also able to metabolize xenobiotics (S)- indan-1-ol and trans-1,2-dihydrobenzene-1,2-diols (PubMed:8573067, PubMed:9716498). 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, PubMed:21802064). |
| Cellular Location | Cytoplasm, cytosol. |
| Tissue Location | Expressed in fetal testes. Expressed in fetal and adult adrenal glands. |
Research Areas
For Research Use Only. Not For Use In Diagnostic Procedures.
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Works in concert with the 5-alpha/5-beta-steroid reductases to convert steroid hormones into the 3-alpha/5-alpha and 3-alpha/5-beta-tetrahydrosteroids. Catalyzes the inactivation of the most potent androgen 5-alpha-dihydrotestosterone (5-alpha- DHT) to 5-alpha-androstane-3-alpha,17-beta-diol (3-alpha-diol). Has a high bile-binding ability.
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