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In addition, treatment prevents mitochondrial nicotinamide-adenine dinucleotide phosphate hydrate (NADPH)-linked substrate depletion and NADPH spontaneous oxidation, making them suitable antioxidants with potential use in atherosclerosis susceptible conditions (84)

Next, to test if PTPN22 drive these functions in a catalytic activity-independent manner, we overexpressed either wild-type or catalytic dead mutant of PTPN22 (Fig

Chen D, Tavana O, Chu B et al (2017) NRF2 Is a major target of ARF in p53-Independent tumor suppression

doi: 10.1016/S0899-9007(00)00244-6, 123

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