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. 2019 Oct 18;28(23):3940–3953. doi: 10.1093/hmg/ddz230

Figure 1.

Figure 1

Smcr8 downregulation in C9ALS/FTD and mutant mouse generation. (A) Western blot analysis of protein expression in spinal cords. β-Actin serves as the loading control. (B) Quantification of protein levels of Smcr8 and other proteins in spinal cords. (C) RT-PCR analysis of Smcr8 mRNA expression. (D) Western blot analysis of the protein expression of Smcr8, C9orf72 and Atg101 in C9ALS/FTD patient brain tissues. β-Actin serves as the loading control. (E) Diagram of the generation of Smcr8−/− mutant mice. (F) Western blot analysis confirmed the absence of Smcr8 protein in mutant mice. β-actin serves as the loading control. (G) LacZ staining of coronal sections from 2-month-old heterozygous mice shows Smcr8 expression in spinal cord. Scale bars: 100 μm. Data are presented as mean ± SEM from three independent experiments containing one WT and one mutant mice in each experiment (n = 3). Statistical analyses were performed with one-way ANOVA with Bonferroni’s post hoc test (***P < 0.001, n.s. represents no significant difference detected).