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This results in impaired mitochondrial integrity, impaired defense against ROS and imbalances in protein homeostasis

However, no such shift was observed in the NE-bound dDAT structure (Fig

Group 2: CPL

These results suggest that perturbation of the malate/aspartate shuttle results in cytosolic retention of NADH and reductive stress, decreasing NADH availability in mitochondria and possibly increasing NAD + levels in the cytosol, thereby leading to inhibition of NADH-dependent mitochondrial respiration and enhancement of NAD + -dependent glycolysis

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