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Effects of presenilin-1 exon 9 deletion and L250S mutations on hyperosmotic stress-induced apoptosis and caspase activities in SH-SY5Y neuroblastoma cells

✍ Scribed by Richard F. Cowburn; Atsuo Sekiyama; Hisashi Tanii; Camilla Nilsberth; Bengt Winblad; Eirikur Benedikz; Maria Ankarcrona


Book ID
117411223
Publisher
Elsevier Science
Year
2000
Tongue
English
Weight
160 KB
Volume
21
Category
Article
ISSN
0197-4580

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## Abstract Presenilins (PSs) are mutated in a majority of familial Alzheimer disease (FAD) cases. Mutated PSs may cause FAD by a number of pro‐apoptotic mechanisms, or by regulating γ‐secretase activity, a protease involved in β‐amyloid precursor protein processing to the neurotoxic β‐amyloid pept