Supplementary Materials

Supplementary Materials for:

Phosphorylation of amyloid precursor protein by mutant LRRK2 promotes AICD activity and neurotoxicity in Parkinson's disease

Zhong-Can Chen, Wei Zhang, Ling-Ling Chua, Chou Chai, Rong Li, Lin Lin, Zhen Cao, Dario C. Angeles, Lawrence W. Stanton, Jian-He Peng, Zhi-Dong Zhou, Kah-Leong Lim, Li Zeng,* Eng-King Tan*

*Corresponding author. Email: li_zeng{at}nni.com.sg (L.Z.); tan.eng.king{at}sgh.com.sg (E.-K.T.)

This PDF file includes:

  • Fig. S1. LRRK2 phosphorylates APP at Thr668.
  • Fig. S2. G2019S mutation in LRRK2 stimulates AICD abundance.
  • Fig. S3. There was no TH loss in the 12-month-old LRRK2G2019S mice.
  • Fig. S4. Expression and wide diffusion of lentiviral AICD in striatum.
  • Fig. S5. Characterization of iPSC-derived human DA neurons.
  • Fig. S6. Dose-dependent study of LRRK2-IN-1 in human LRRK2G2019S neurons.
  • Fig. S7. AICD-associated TH loss in 20-month-old LRRK2G2019S mice is selective to DA neurons in the SN.

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Citation: Z.-C. Chen, W. Zhang, L.-L. Chua, C. Chai, R. Li, L. Lin, Z. Cao, D. C. Angeles, L. W. Stanton, J.-H. Peng, Z.-D. Zhou, K.-L. Lim, L. Zeng, E.-K. Tan, Phosphorylation of amyloid precursor protein by mutant LRRK2 promotes AICD activity and neurotoxicity in Parkinson's disease. Sci. Signal. 10, eaam6790 (2017).

© 2017 American Association for the Advancement of Science