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. Author manuscript; available in PMC: 2022 Dec 1.
Published in final edited form as: Neuron. 2021 Oct 12;109(23):3758–3774.e11. doi: 10.1016/j.neuron.2021.09.031

Figure 5. TRIP12 Knockout Rescues α-syn PFFs-induced Pathologies in Human Dopaminergic (DA) Neurons.

Figure 5

(A) Western blot analysis of TRIP12 and GCase in conditionally floxed TRIP12 hESCs-derived human dopaminergic (DA) neurons transduced with AAV expressing either control (TRIP12flox/flox) or cre recombinase (TRIP12flox/flox;Cre) and treated with PBS or α-syn PFFs.

(B) Data in A shown as bar graphs (n=4, each group).

(C) GCase activity (n=6, each group).

(D) GBA1 mRNA level (n=6, each group).

(E) Representative confocal images showing p-α-syn aggregates.

(F) Data in E shown as bar graphs (n=6, each group).

(G) The p-α-syn positive signals co-localize with ubiquitin.

(H) Western blot analysis of α-syn, p-α-syn, and β-actin from TX-soluble and TX-insoluble fractions.

(I) Bar graph of the levels of α-syn aggregates and p-α-syn in TX-insoluble fraction (n=3, each group).

(J) Quantification of AlamarBlue assay (n=6, each group).

(K) LDH assay (n=6, each group). Data are presented as mean ± SEM (NS; not significant, *P < 0.05, **P < 0.01, ***P < 0.001).

See also Figure S6.