Gain-of-function enhancement of IP3 receptor modal gating by familial Alzheimer's disease-linked presenilin mutants in human cells and mouse neurons.

@article{Cheung2010GainoffunctionEO,
  title={Gain-of-function enhancement of IP3 receptor modal gating by familial Alzheimer's disease-linked presenilin mutants in human cells and mouse neurons.},
  author={King-Ho Cheung and Lijuan Mei and Don-On Daniel Mak and Ikuo Hayashi and Takeshi Iwatsubo and David E. Kang and J. Kevin Foskett},
  journal={Science signaling},
  year={2010},
  volume={3 114},
  pages={ra22}
}
Familial Alzheimer's disease (FAD) is caused by mutations in amyloid precursor protein or presenilins (PS1 and PS2). Many FAD-linked PS mutations affect intracellular calcium (Ca(2+)) homeostasis by mechanisms proximal to and independent of amyloid production, although the molecular details are controversial. We found that several FAD-causing PS mutants enhance gating of the inositol trisphosphate receptor (IP(3)R) Ca(2+) release channel by a gain-of-function effect that mirrored the genetics… CONTINUE READING

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  • I. Schneider Herms, I. Dewachter, N. Caluwaerts, H. Kretzschmar, F. Van Leuven
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