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. Author manuscript; available in PMC: 2022 Mar 1.
Published in final edited form as: Mov Disord. 2020 Oct 26;36(2):348–359. doi: 10.1002/mds.28346

Figure 2. Inhibition of APT1 reduces pSer129 αS.

Figure 2.

(A) IF for neuronal markers demonstrates the neuronal phenotype of human iN cells derived from the 2132 wt iPSC line. Scale bar, 50 μm. (B) IF for neuronal markers in YZ1 human iN cells. Scale bar, 50 μm. (C) APT1 inhibition in human neurons reduces αS phosphorylated at S129 (pSer129 αS). iNs expressing vector only, αS wt or E46K at DIV18 were treated with the indicated doses of ML348 for 48 hr. Shown are a representative result (left) and quantification (right). pSer129 αS band intensity was normalized to total αS and expressed as percentage of the untreated DMSO vehicle control. (N = 5). (D) Analogous to c using iNs derived from the YZ1 iPSC line. (N = 4). (E) pSer129 αS was measured by WB in iNs expressing αS wt, E46K, or 3K, expressed as a ratio of pSer129 αS to total αS. (N = 4). (F) APT1 knockdown in human neurons reduces pSer129 αS. iNs were transfected with dsiRNA against APT1 and pSer129 αS measured as in (B). (wt, N = 5; E46K, N = 7). All data are means ± s.e.m. Criteria for significance relative to DMSO or NC5 negative control dsiRNA were *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.