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. Author manuscript; available in PMC: 2020 Dec 4.
Published in final edited form as: Neuron. 2019 Oct 21;104(5):869–884.e11. doi: 10.1016/j.neuron.2019.09.001

Figure 6. FTIs enhance lysosomal GCase activity and reduce pathological a-syn by blocking ykt6 farnesylation.

Figure 6.

A) GCase activity in FTI-treated A53T iPSn at d80 (LNK-754 5nM, 5d). B) GCase activity in FTI-treated A53T iPSn expressing empty vector (vect) or ykt6-CS (n=4). C) Lysosomal GCase activity was assessed in FTI-treated SH-SY5Y cells transfected with scrambled or ykt6 shRNA (KD) (n=3). D) Quantification of Triton X-100 soluble (T-sol) a-syn by western blot from FTI-treated A53T iPSn (5nM, 7d). *, non-specific band. (n=3). E) Quantification of insoluble a-syn from A53T iPSn as in D (n=3). F) Insoluble a-syn in FTI-treated H4 cells (5nM, 5 days) transfected with either scrambled or ykt6 shRNA (n=6). G) Neuron viability was assessed in FTI-treated A53T iPSn (5nM, 14d from d86-d100) by quantification of neurofilament protein. Right, neuron viability in FTI-treated A53T iPSn expressing empty vector or ykt6-CS (n=4). Values are the mean +/− SEM, *p<0.05, **p<0.01, ***p<0.001. The dashed line indicates cropped out replicates. See also Figure S6.