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• W2012793141 startingPage "365" @default.
• W2012793141 abstract "The involvement of tau phosphorylation in apoptosis resembling Alzheimer's disease (AD) was investigated using a cell model of P19 cells stably expressing human tau441 (tau/P19 cells). Apoptotic cell death was observed specifically in tau/P19 cells during neural differentiation with retinoic acid (RA) treatment. A CaM kinase II inhibitor, KN-93, protected tau/P19 cells from apoptosis, although it stimulated the cell death of wild-type P19 cells (wt/P19 cells). W-7 and calmidazolium, calmodulin antagonists, also specifically inhibited the apoptosis of tau/P19 cells. LiCl, an inhibitor of glycogen synthase 3, a tau kinase, was effective in protecting tau/P19 cells from apoptosis, but the protective effect was less than that of CaM kinase II inhibitor and calmodulin antagonists. Tau in the nuclei of tau/P19 cells was phosphorylated at the sites for CaM kinase II detected by an antibody recognizing a phosphorylated form of tau. These results indicated that CaM kinase II was involved in the apoptosis of tau/P19 cells induced by RA treatment." @default.
• W2012793141 created "2016-06-24" @default.
• W2012793141 creator A5008405377 @default.
• W2012793141 creator A5074838349 @default.
• W2012793141 date "2009-04-01" @default.
• W2012793141 modified "2023-09-25" @default.
• W2012793141 title "Ca^{2 +}/calmodulin-dependent protein kinase II mediates apoptosis of P19 cells expressing human tau during neural differentiation with retinoic acid treatment" @default.
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• W2012793141 doi "https://doi.org/10.1080/14756360802187851" @default.
• W2012793141 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18830878" @default.
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