Abstract
The expression of the carboxyl-terminal 100 (C-100) residues of the amyloid precursor protein (APP) may provide a model for studying the processing of APP to the 42–43 residue β-amyloid peptide (βA4) implicated in Alzheimer's disease. Expression of human C-100 in mammalian cells reportedly causes ‘toxicity’ and amyloid-like fibrils. We have expressed the C-100 fragment in human embryonic kidney cells (293 cells) in a transient assay and compared it to the expression of transfected wild type and mutant (Swedish familial Alzheimer's disease) full length APP. Products were characterized by Western blot analysis using antibodies to the carboxyl-terminal region of APP.
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