Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder. In the present study, the function of amyloid precursor protein (APP) in modulating capacitive calcium entry (CCE), a refilling mechanism for depleted intracellular calcium stores, was investigated. CCE in neural 2a (N2a) cells stably expressing wild-type human APP was lower than in wild-type N2a cells, while CCE in APP knockout mouse embryonic fibroblast (MEF) cells was higher than in their wild-type counterparts. We demonstrate that wild-type APP depresses CCE. Furthermore, using N2a cells transfected with C-terminal APP fragments, we show that these fragments anchored in the cell membrane play an important role in CCE depression.
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