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The role of SOD1 mutation on copper dys-regulation in neurodegenerative disorders, particularly in ALS has been noticed by some researchers

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The methods of intervention are diverse, encompassing direct binding, the regulation of expression, and functional activation, which positions FDX1 as a highly attractive drug target

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This was supported by structural biology studies which described how the membrane binding regions of PPOX can be docked onto FECH, potentially enabling a direct transfer of reactants from the active site of PPOX to that of FECH (Koch et al., 2004)