Additional file 1 of Recombinant SMN protein synergizes with spinal muscular atrophy therapy to counteract pathological motor neuron phenotypes

Additional file 1. Figure S1. Evaluation of recombinant TAT-flSMN folding and oligomerization states. Figure S2. Deconvoluted MS/MS spectrum of the 2+ charged ion at m/z 1156.5177 (precursor mass deviation: -0.7 ppm; retention time: 110.36 min). Figure S3. Deconvoluted MS/MS spectrum of the 3+ charged ion at m/z 887.4210 (precursor mass deviation: 2.4 ppm; retention time 198.2 min). Figure S4. Deconvoluted MS/MS spectrum of the 3+ charged ion at m/z 585.6333 (precursor mass deviation: -2.7 ppm; retention time: 36.359 min). Figure S5. Effect of SMN depletion on neurite outgrowth and cell death in differentiated NSC-34 motor neuronal cells. Figure S6. Impact of PMO25 on NSC-34 cells expressing SMN-reporter mini-genes and human SMA fibroblasts. Figure S7. iPSC differentiation into mature, electrophysiologically active motor neurons. Figure S8. Impact of SMN deficiency on SMA iPSC properties. Figure S9. TAT-flSMN and PMO25 induce neurite elongation and prevent apoptotic cell death on SMA iPSC-derived MNs. Table S1. Summary of SAXS data analysis. Supplementary Materials and Methods.