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- 技术资料
- 规格:
100ul
| 产品编号 | bs-24205R-Bio |
| 英文名称 | HSD3B2 Rabbit pAb, Biotin conjugated |
| 中文名称 | Biotin标记的3β-羟基类固醇脱氢酶/δ5->4-异构酶2型抗体 |
| 英文别名 | 3BHS2_HUMAN; 3 beta-hydroxysteroid dehydrogenase/delta 5-->4-isomerase type 2; 3 beta-hydroxysteroid dehydrogenase/delta 5-->4-isomerase type II(3-beta-HSD II); 3-beta-HSD adrenal and gonadal type; 3-beta-hydroxy-delta(5)-steroid dehydrogenase; EC:1.1.1.145; EC:1.1.1.145; Progesterone reductase; Steroid delta-isomerase; EC:5.3.3.1; delta-5-3-ketosteroid isomerase; HSDB3B; HSDB; HSD3B; SDR11E2; |
| 产品应用 | WB=1:500-2000 Not yet tested in other applications. |
| 抗体来源 | Rabbit |
| 免疫原 | KLH conjugated synthetic peptide derived from mouse HSD3B2 |
| 亚型 | IgG |
| 纯化方法 | affinity purified by Protein A |
| 克隆类型 | Polyclonal |
| 浓度 | 1mg/ml |
| 储存液 | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| 亚基 | Expressed in adrenal gland, testis and ovary. |
| 亚细胞定位 | Endoplasmic reticulum membrane. Mitochondrion membrane. |
| 组织特异性 | Defects in HSD3B2 are the cause of adrenal hyperplasia type 2 (AH2) [MIM:201810]. AH2 is a form of congenital adrenal hyperplasia, a common recessive disease due to defective synthesis of cortisol. Congenital adrenal hyperplasia is characterized by androgen excess leading to ambiguous genitalia in affected females, rapid somatic growth during childhood in both sexes with premature closure of the epiphyses and short adult stature. Four clinical types: 'salt wasting' (SW, the most severe type), 'simple virilizing' (SV, less severely affected patients), with normal aldosterone biosynthesis, 'non-classic form' or late onset (NC or LOAH), and 'cryptic' (asymptomatic). In AH2, virilization is much less marked or does not occur. AH2 is frequently lethal in early life. _x000D_ Note=Mild HSD3B2 deficiency in hyperandrogenic females is associated with characteristic traits of polycystic ovary syndrome, such as insulin resistance and luteinizing hormon hypersecretion. |
| 相似性 | Belongs to the 3-beta-HSD family. |
| 功能 | 3-beta-HSD is a bifunctional enzyme, that catalyzes the oxidative conversion of Delta(5)-ene-3-beta-hydroxy steroid, and the oxidative conversion of ketosteroids. The 3-beta-HSD enzymatic system plays a crucial role in the biosynthesis of all classes of hormonal steroids. |
| 保存条件 | Shipped at 4℃. Store at -20°C for one year. Avoid repeated freeze/thaw cycles. |
| 注意事项 | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| 背景资料 | Predicted to enable 3-beta-hydroxy-delta5-steroid dehydrogenase activity and steroid delta-isomerase activity. Predicted to be involved in several processes, including hippocampus development; response to corticosterone; and steroid hormone biosynthetic process. Predicted to be located in several cellular components, including intercellular bridge; mitochondrial envelope; and nucleolus. Predicted to be active in cytoplasm and intracellular membrane-bounded organelle. Is expressed in liver. Human ortholog(s) of this gene implicated in hypertension and hypospadias. Orthologous to human HSD3B1 (hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1) and HSD3B2 (hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 2). [provided by Alliance of Genome Resources, Apr 2022] Function : 3-beta-HSD is a bifunctional enzyme, that catalyzes the oxidative conversion of Delta(5)-ene-3-beta-hydroxy steroid, and the oxidative conversion of ketosteroids. The 3-beta-HSD enzymatic system plays a crucial role in the biosynthesis of all classes of hormonal steroids. Subunit : Expressed in adrenal gland, testis and ovary. Subcellular Location : Endoplasmic reticulum membrane. Mitochondrion membrane. Tissue Specificity : Defects in HSD3B2 are the cause of adrenal hyperplasia type 2 (AH2) [MIM:201810]. AH2 is a form of congenital adrenal hyperplasia, a common recessive disease due to defective synthesis of cortisol. Congenital adrenal hyperplasia is characterized by androgen excess leading to ambiguous genitalia in affected females, rapid somatic growth during childhood in both sexes with premature closure of the epiphyses and short adult stature. Four clinical types: 'salt wasting' (SW, the most severe type), 'simple virilizing' (SV, less severely affected patients), with normal aldosterone biosynthesis, 'non-classic form' or late onset (NC or LOAH), and 'cryptic' (asymptomatic). In AH2, virilization is much less marked or does not occur. AH2 is frequently lethal in early life. Note=Mild HSD3B2 deficiency in hyperandrogenic females is associated with characteristic traits of polycystic ovary syndrome, such as insulin resistance and luteinizing hormon hypersecretion. DISEASE : Defects in HSD3B2 are the cause of adrenal hyperplasia type 2 (AH2) [MIM:201810]. AH2 is a form of congenital adrenal hyperplasia, a common recessive disease due to defective synthesis of cortisol. Congenital adrenal hyperplasia is characterized by androgen excess leading to ambiguous genitalia in affected females, rapid somatic growth during childhood in both sexes with premature closure of the epiphyses and short adult stature. Four clinical types: 'salt wasting' (SW, the most severe type), 'simple virilizing' (SV, less severely affected patients), with normal aldosterone biosynthesis, 'non-classic form' or late onset (NC or LOAH), and 'cryptic' (asymptomatic). In AH2, virilization is much less marked or does not occur. AH2 is frequently lethal in early life. Note=Mild HSD3B2 deficiency in hyperandrogenic females is associated with characteristic traits of polycystic ovary syndrome, such as insulin resistance and luteinizing hormon hypersecretion Similarity : Belongs to the 3-beta-HSD family. SWISS: P26439 Gene ID : 3284 Human Gene ID : 3284 Database links : Entrez Gene: 3284 Human Entrez Gene: 15493 Mouse Entrez Gene: 29632 Rat SwissProt: P26439 Human SwissProt: P26149 Mouse |
| 应用 | 推荐稀释比例 |
| {WB} | {1:500-2000} |
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Hsd3b2 | 3-beta-HSD2 Rabbit pAb, Biotin conj.(bs-24205R-Bio)-100ul
¥2980






