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. 2017 Mar 30;7:46. doi: 10.3389/fonc.2017.00046

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Copyright © 2017 Schrier, Trivedi and Deth.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Nrf2-dependent transcription of genes promoting GSH synthesis. Oxidative stress induces the dissociation of Nrf2 from cytosolic Keap1, allowing its relocation to the nucleus where it augments the transcription of multiple genes directly or indirectly involved in GSH synthesis (dashed arrows), thereby increasing antioxidant capacity. Nrf2 activation of GSH synthesis negatively affects the methylation capacity by promoting transsulfuration of homocysteine to cysteine. Abbreviations: CBS, cystathionine-β-synthase; CGL, cystathionine-γ-lyase, EAAT3, excitatory amino acid transporter-3; GCLM, γ-glutamylcysteine ligase modulatory subunit; GR, glutathione reductase; GSH, glutathione; GSS, glutathione synthetase; GSSG, glutathione disulfide; G6PD, glucose-6-phosphate dehydrogenase; Keap1, kelch-like ECH-associated protein 1; Maf, musculoaponeurotic fibrosarcoma proteins; MAT, methionine adenosyltransferase; MS, methionine synthase; MT, methyltransferase; Nrf2, nuclear factor (erythroid-derived 2)-like 2; SAHH, S-adenosylhomocysteine hydrolase.