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To remove excess amounts of deleterious ROS, neurons rely on oxidative phosphorylation and antioxidants such as glutathione (GSH)

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While some of these, like OTUB2, are predicted to be inactive, resulting from the absence of the negatively charged member of the catalytic triad to polarize the histidine, tumor necrosis factor alpha–induced protein 3 (A20) has been demonstrated to retain activity after an induced mutation of its catalytic aspartate residue (60, 61)