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PS2 mutation increases neuronal cell vulnerability to neurotoxicants through activation of caspase-3 by enhancing of ryanodine receptor-mediated calcium release

College of Pharmacy, Chungbuk National University, Chungbuk, Korea.
The FASEB Journal (Impact Factor: 5.48). 02/2006; 20(1):151-3. DOI: 10.1096/fj.05-4017fje;1
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    • "Furthermore , we have demonstrated that PS1 influences the structural plasticity of postsynaptic dendritic spines in the somatosensory cortex (Jung et al., 2011). FAD-PS mutations have been shown to increase the neuronal vulnerability to A␤ and glutamate through caspase-3 activation as a result of RyR3 isoform upregulation and enhanced RyR-mediated calcium release in PC12 cells (Lee et al., 2006). Notably, the FAD-PS mediated vulnerability and apoptosis can be normalized by pharmacologically or functionally inhibiting the IP 3 R-CaMKIV-CREB pathway in SH-SY5Y cells (Muller et al., 2011). "
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    • "The data in cultured neurons indicate that, while in cells from tg mice activation of IP 3 -Rs results in an attenuated Ca 2+ peak, the response to Ry-Rs is increased. It has been demonstrated that in other AD mouse models based on PS mutants, the expression level of Ry-Rs is enhanced compared with wt animals (Lee et al., 2006; Stutzmann et al., 2007). "
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