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Additional file 9: Figure S9. of α-Synuclein accumulation and GBA deficiency due to L444P GBA mutation contributes to MPTP-induced parkinsonism

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posted on 2018-01-08, 05:00 authored by Seung Yun, Donghoon Kim, Sangjune Kim, SangMin Kim, Senthilkumar Karuppagounder, Seung-Hwan Kwon, Saebom Lee, Tae-In Kam, Suhyun Lee, Sangwoo Ham, Jae Park, Valina Dawson, Ted Dawson, Yunjong Lee, Han Ko
L444P GBA heterozygous mutation leads to autophagy abnormality. a, b Effect of rapamycin on GBA +/L444P expression. Primary cortical neurons were cultured from WT and GBA +/L444P mice. After 10 DIV, primary neurons were treated with 20 nM of rapamycin (mTOR inhibitor for inducing autophagy) for 24 h. a Representative Immunoblots of GBA. b GBA expression levels were normalized against β-actin and the error bars represent the mean ± S.E.M (n = four per group). c Immunoblots of Autophagy marker proteins SQSTM1/p62, and LC3A/B-I/II. VMB lysates were immunoblotted with anti-SQSTM1/p62, and anti-LC3A/B-I/II antibodies. d SQSTM1/p62, and e LC3A/B-II expression levels were normalized against β-actin. Error bars represent the mean ± S.E.M (n = four mice per group). Two-way ANOVA was used for statistical analysis followed by post-hoc Bonferroni test for multiple group comparison. *P < 0.05, **P < 0.01, ***P < 0.001. n.s: not significant. (PDF 338 kb)

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Morris K. Udall Parkinson’s Disease Research Center

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