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。
ALAS2 Antibody (monoclonal) (M02)
Mouse monoclonal antibody raised against a partial recombinant ALAS2.
- 产品详情
- 实验流程
- 背景知识
Application 
| WB, E |
|---|---|
| Primary Accession | P22557 |
| Other Accession | NM_000032 |
| Reactivity | Human, Mouse |
| Host | mouse |
| Clonality | monoclonal |
| Isotype | IgG2a Kappa |
| Clone Names | 4D8 |
| Calculated MW | 64633 Da |
| Gene ID | 212 |
|---|---|
| Other Names | 5-aminolevulinate synthase, erythroid-specific, mitochondrial, ALAS-E, 5-aminolevulinic acid synthase 2, Delta-ALA synthase 2, Delta-aminolevulinate synthase 2, ALAS2, ALASE, ASB |
| Target/Specificity | ALAS2 (NP_000023, 1 a.a. ~ 100 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. |
| Dilution | WB~~1:500~1000 |
| Format | Clear, colorless solution in phosphate buffered saline, pH 7.2 . |
| Storage | Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. |
| Precautions | ALAS2 Antibody (monoclonal) (M02) is for research use only and not for use in diagnostic or therapeutic procedures. |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
The product of this gene specifies an erythroid-specific mitochondrially located enzyme. The encoded protein catalyzes the first step in the heme biosynthetic pathway. Defects in this gene cause X-linked pyridoxine-responsive sideroblastic anemia. Alternatively spliced transcript variants encoding different isoforms have been identified.
REFERENCES
Systematic molecular genetic analysis of congenital sideroblastic anemia: evidence for genetic heterogeneity and identification of novel mutations. Bergmann AK, et al. Pediatr Blood Cancer, 2010 Feb. PMID 19731322.Hypoxia induces erythroid-specific 5-aminolevulinate synthase expression in human erythroid cells through transforming growth factor-beta signaling. Kaneko K, et al. FEBS J, 2009 Mar. PMID 19187226.Multi-organ iron overload in an African-American man with ALAS2 R452S and SLC40A1 R561G. Sussman NL, et al. Acta Haematol, 2008. PMID 19066423.C-terminal deletions in the ALAS2 gene lead to gain of function and cause X-linked dominant protoporphyria without anemia or iron overload. Whatley SD, et al. Am J Hum Genet, 2008 Sep. PMID 18760763.Lack of association of delta-aminolevulinate dehydratase polymorphisms with blood lead levels and hemoglobin in Romanian women from a lead-contaminated region. Rabstein S, et al. J Toxicol Environ Health A, 2008. PMID 18569569.
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