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Mechanisms of cuproptosis, a Cu-dependent form of programmed cell death. Cu2+ accumulating in mitochondria is reduced to a more toxic Cu + by FDX1. FDX1 also promotes lipoylation of proteins including DLAT by up-regulation of LIAS. Binding Cu + to lipoylated DLAT (DLAT-LA) induces protein aggregation. The latter results in proteotoxic stress that is also associated with Cu-induced loss of Fe-S cluster proteins, altogether leading to cuproptosis.
