摘要
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.
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.
基金
supported by the State Key Laboratory of Biomembrane and Membrane Biotechnology
the National Natural Science Foundation of China(NSFC)/Research Grants Council of Hong Kong(RGC) Joint Research Scheme(81161160570)
Tsinghua-Yue-Yuen Medical Sciences Fund(20240000514)
