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. Author manuscript; available in PMC: 2022 May 19.
Published in final edited form as: J Am Chem Soc. 2021 Apr 15;143(19):7368–7379. doi: 10.1021/jacs.1c00131

Figure 5.

Figure 5.

Reduction in poly-GP by knockdown of DHX36 in patient-derived iPSCs and iMNs and upregulation of DHX36 in the spinal cords of C9orf72-linked ALS patients. (A) C9orf72-linked ALS patient-derived iPSCs were analyzed for poly-GP levels by ELISA, with or without the stable knockdown of DHX36. Data are given as means ± SD of four replicates from two independent experiments. **P < 0.01, ***P < 0.001. (B) C9orf72-linked ALS patient-derived iMNs were analyzed for poly-GP levels by ELISA, with or without the stable knockdown of DHX36. Data are given as means ± SD of four replicates from two independent experiments. ***P < 0.001, ****P < 0.0001. (C) DHX36 protein expression levels are higher in the spinal cord tissues from C9orf72-linked ALS patients than in the controls. Data are given as means ± SD of samples from five patients or five controls. *P = 0.0335.