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The study found that for erastin-induced GLCM, xCT, FTH1, FTL, and FPN1, and other antioxidant system and iron metabolism-related proteins, BACH1 inhibited the transcription of their coding genes and promoted ferroptosis (Nishizawa et al
Pathmeswaran, A
Tong J, Ang L-C, Williams B, Furukawa Y, Fitzmaurice P, Guttman M, Boileau I, Hornykiewicz O, Kish SJ
Glut4 mobilization supports energetic demands of active synapses
More toxins further impair methylation, and impaired methylation slows clearance even more
Multifunctional roles of enolase in Alzheimer's disease brain: beyond altered glucose metabolism
