Supplementary Materials

Supplementary Materials for:

Familial Alzheimer's disease–associated presenilin 1 mutants promote γ-secretase cleavage of STIM1 to impair store-operated Ca2+ entry

Benjamin Chun-Kit Tong, Claire Shuk-Kwan Lee, Wing-Hei Cheng, Kwok-On Lai, J. Kevin Foskett, King-Ho Cheung*

*Corresponding author. Email: kingho.cheung{at}hku.hk

This PDF file includes:

  • Fig. S1. Mutant PS1 or PS1 knockout does not grossly affect STIM1 or ORAI1 abundance in SH-SY5Y cells.
  • Fig. S2. Impaired CCE in mutant FAD-PS1–expressing cells or PS1 knockout cells.
  • Fig. S3. PS1 interacts with STIM1 but not with CFTR.
  • Fig. S4. In situ PLA demonstrates that endogenous PS1 and STIM1 interact.
  • Fig. S5. FAD-linked mutant PS1 impairs STIM1 puncta formation.
  • Fig. S6. Mutant PS1 attenuates the STIM1-ORAI1 interaction in fibroblasts from FAD patients.
  • Fig. S7. In vitro fluorogenic γ-secretase cleavage assay.
  • Table S1. The effects of PS1 on CCE.
  • Table S2. The amount of PLA red fluorescent dots in SH-SY5Y cells.
  • Table S3. The effects of PS1 on the STIM1-ORAI1 interaction after ER Ca2+ depletion by thapsigargin.
  • Table S4. The effects of PS1 on spine stability in isolated rat hippocampal neurons.

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Citation: B. C.-K. Tong, C. S.-K. Lee, W.-H. Cheng, K.-O. Lai, J. Kevin Foskett, K.-H. Cheung, Familial Alzheimer's disease&ndashl;associated presenilin 1 mutants promote γ-secretase cleavage of STIM1 to impair store-operated Ca2+ entry. Sci. Signal. 9, ra89 (2016).

© 2016 American Association for the Advancement of Science