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NRF2 is the master switch of the cellular antioxidant response: when oxidative stress is sensed, KEAP1 (the NRF2 repressor) is oxidized at critical cysteine residues, releasing NRF2 for nuclear translocation and ARE-driven upregulation of the complete antioxidant gene set including GCLC, GCLM, GSR, GPX1, GSTP1, and the thioredoxin system

a phenomenon that in WT cells is overtime counteracted by homeoviscous adaptation restoring membrane fluidity close to preshift levels

Each dimer of IDH has two active sites

It is either synthesized from -glutamyl-cysteine and glycine by glutathione synthetase (GSS) or recycled from glutathione disulfide by glutathione reductase (GSR) using NADPH as a reducing agent [33]

Yes, perimenopause and menopause can act as a trigger for the onset of autoimmune disease in women who are genetically predisposed or already showing signs of immune dysfunction