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ALDOB Antibody (monoclonal) (M01)
Mouse monoclonal antibody raised against a full length recombinant ALDOB.
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| E |
|---|---|
| Primary Accession | P05062 |
| Other Accession | BC029399 |
| Reactivity | Human |
| Host | mouse |
| Clonality | Monoclonal |
| Isotype | IgG2a kappa |
| Clone Names | 3B3 |
| Calculated MW | 39473 Da |
| Gene ID | 229 |
|---|---|
| Other Names | Fructose-bisphosphate aldolase B, Liver-type aldolase, ALDOB, ALDB |
| Target/Specificity | ALDOB (AAH29399, 1 a.a. ~ 316 a.a) full-length recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. |
| 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 | ALDOB Antibody (monoclonal) (M01) is for research use only and not for use in diagnostic or therapeutic procedures. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Fructose-1,6-bisphosphate aldolase (EC 4.1.2.13) is a tetrameric glycolytic enzyme that catalyzes the reversible conversion of fructose-1,6-bisphosphate to glyceraldehyde 3-phosphate and dihydroxyacetone phosphate. Vertebrates have 3 aldolase isozymes which are distinguished by their electrophoretic and catalytic properties. Differences indicate that aldolases A, B, and C are distinct proteins, the products of a family of related 'housekeeping' genes exhibiting developmentally regulated expression of the different isozymes. The developing embryo produces aldolase A, which is produced in even greater amounts in adult muscle where it can be as much as 5% of total cellular protein. In adult liver, kidney and intestine, aldolase A expression is repressed and aldolase B is produced. In brain and other nervous tissue, aldolase A and C are expressed about equally. There is a high degree of homology between aldolase A and C. Defects in ALDOB cause hereditary fructose intolerance.
References
The biochemical basis of hereditary fructose intolerance. Bouteldja N, et al. J Inherit Metab Dis, 2010 Apr. PMID 20162364.Increased prevalence of mutant null alleles that cause hereditary fructose intolerance in the American population. Coffee EM, et al. J Inherit Metab Dis, 2010 Feb. PMID 20033295.Secreted protein acidic and rich in cysteine (SPARC) gene polymorphism association with hepatocellular carcinoma in Italian patients. Segat L, et al. J Gastroenterol Hepatol, 2009 Dec. PMID 19817957.Five mucosal transcripts of interest in ulcerative colitis identified by quantitative real-time PCR: a prospective study. Eriksson A, et al. BMC Gastroenterol, 2008 Aug 12. PMID 18700007.Hereditary fructose intolerance: frequency and spectrum mutations of the aldolase B gene in a large patients cohort from France--identification of eight new mutations. Davit-Spraul A, et al. Mol Genet Metab, 2008 Aug. PMID 18541450.
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