| 產(chǎn)品編號(hào) | bs-16552R |
| 英文名稱 | Rabbit Anti-HSD3B2 antibody |
| 中文名稱 | 3β-羥基類固醇脫氫酶/δ5->4-異構(gòu)酶2型抗體 |
| 別 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; |
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Specific References (1) | bs-16552R has been referenced in 1 publications.
[IF=2.445] Ma Z et al. Neuromedin B regulates steroidogenesis, cell viability and apoptosis in rabbit Leydig cells. Gen Comp Endocrinol. 2019 Dec 16;288:113371. WB&IHC-P,ICF ; Rabbit.
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| 研究領(lǐng)域 | 細(xì)胞生物 信號(hào)轉(zhuǎn)導(dǎo) 生長(zhǎng)因子和激素 新陳代謝 線粒體 |
| 抗體來(lái)源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | Rat (predicted: Human,Pig,Dog) |
| 產(chǎn)品應(yīng)用 | IHC-P=1:100-500,IHC-F=1:100-500,ICC/IF=1:100-500,IF=1:100-500,ELISA=1:5000-10000
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 理論分子量 | 40kDa |
| 細(xì)胞定位 | 細(xì)胞漿 線粒體 |
| 性 狀 | Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human HSD3B2 |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 緩 沖 液 | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| 保存條件 | Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles. |
| 注意事項(xiàng) | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| PubMed | PubMed |
| 產(chǎn)品介紹 |
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 Database links: Entrez Gene: 3284 Human Entrez Gene: 15493 Mouse SwissProt: P26439 Human SwissProt: P26149 Mouse |
| 產(chǎn)品圖片 |
Paraformaldehyde-fixed, paraffin embedded (rat ovary tissue); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30min; Antibody incubation with (HSD3B2) Polyclonal Antibody, Unconjugated (bs-16552R) at 1:400 overnight at 4°C, followed by operating according to SP Kit(Rabbit) (sp-0023) instructionsand DAB staining.
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