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 E~~N/A |
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. |
For Research Use Only. Not For Use In Diagnostic 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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