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. Author manuscript; available in PMC: 2015 Oct 29.
Published in final edited form as: Cell. 2014 May 8;157(4):882–896. doi: 10.1016/j.cell.2014.03.026

Figure 7. The NAD+ precursor nicotinamide riboside can rescue the mitochondrial phenotype of CX mice in vivo.

Figure 7

(A) Immunoblot of cerebellar proteins in 3-month old WT and CX mice treated with saline or nicotinamide riboside (NR) subcutaneous injections for 2 weeks (500 mg NR/kg body weight). Each lane is a separate mouse. (B) NAD+ levels in the cerebellum of the mice described in (A) (means ± S.D., n=4). (C) The mitochondrial membrane potential of isolated cerebellar mitochondria from mice described in (A) (means ± S.D., n=4). (D) ROS production in isolated cerebellar mitochondria from mice described in (A) (means ± S.D., n=4). (E) ATP levels in the cerebellum of mice as described in (A) (means ± S.D., n=4). (F) Venn diagram of significantly changed gene in the cerebellum when comparing CX-saline with WT-saline and CX-NR treated with WT-saline treated (n=3). (G) An overview of the significantly changed genes when comparing CX-saline vs WT-saline and CX-NR vs WT-saline (n=3). (H) Principal component analysis of the average Z-scores of all the genes in each group (n=3).