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。
HSD3B2 Rabbit pAb
HSD3B2 Rabbit pAb
- 产品详情
- 实验流程
- 背景知识
Application 
| WB |
|---|---|
| Reactivity | Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 40 KDa |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from mouse HSD3B2 |
| Epitope Specificity | 151-250/372 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SUBCELLULAR LOCATION | Endoplasmic reticulum membrane. Mitochondrion membrane. |
| SIMILARITY | Belongs to the 3-beta-HSD family. |
| SUBUNIT | Expressed in adrenal gland, testis and ovary. |
| 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 |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | 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 |
| Target/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. |
|---|---|
| Dilution | WB=1:500-2000 |
| Format | 0.01M TBS(pH7.4) with 1% BSA, 0.09% (W/V) sodium azide and 50% Glyce |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
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
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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