This peptide is the mutant form of beta-Amyloid 1 to 40. These mutations within the beta-Amyloid precursor protein (APP) regions result in the substitution of glutamine for glutamic acid and asparagine for aspartic acid. The peptide rapidly assembles in solution to form fibrils compared to the wild-type beta-Amyloid 1 to 40. Double-mutant E22Q/D23N Dutch/Iowa beta-Amyloid 40 is more potent than either of the single mutant form in causing pathologic responses in culture cells. The double mutations further enhances the fibrillogenic and pathogenic properties of beta-Amyloid.
Proteins & Peptides
Peak Area by HPLC ≥95%
Van Nostrand, W. et al. Ann. N.Y. Acad. Sci. 977, 258 (2002).