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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.