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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 2. TRIP12 Accumulates in Sporadic PD Patients and in PD Mouse Models.

Figure 2

(A) Western blot analysis of TRIP12, GCase, TH, and α-syn protein levels in the SNpc of human PD postmortem brain.

(B) Data in A shown as bar graphs (n=6, each group).

(C) Correlation between TRIP12 and GCase expression (n=6, each group).

(D) GCase activity was measured by inactivating GBA2 protein with CBE treatment in PD postmortem brain and represented in a bar graph (n=6, each group).

(E) GBA1 mRNA levels (n=6, each group).

(F) Western blot analysis of TRIP12, GCase, TH, and α-syn from the VMB of α-syn PFFs-injected mice at 6-months post-injection.

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

(H) Correlation between TRIP12 and GCase expression (n=6, each group).

(I and J) GCase activity and GBA1 mRNA levels (n=6, each group).

(K) Western blot analysis of TRIP12, GCase, and α-syn from the brainstem region of 9 to 10-month-old human A53T α-syn transgenic mice (hA53T-Tg) or age-matched nontransgenic mice (non-Tg).

(L) Data in K shown as bar graphs (n=6, each group).

(M) Correlation between TRIP12 and GCase expression (n=6, each group).

(N and O) GCase activity and GBA1 mRNA levels. Data are presented as mean ± SEM (NS; not significant, *P < 0.05, **P < 0.01, ***P < 0.001).

See also Figure S4 and Table S3.