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Therefore, to further dissociate the effects of GSH and NRF2 on lipid abundance and assess if NRF2 activation alone mimics the effects of liver-specific Gclc deletion, we treated Gclc WT mice with CDDO-methyl (CDDO-Me), a form of bardoxolone with increased bioavailability

We view this structure as an excellent model for Zur-regulated PyrC2 given the high (50%) sequence identity and the presence of the same site 1 Gln substitution that is found in the P