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Evidence from human genetic syndromes substantiates the concept of plasticity, given the congenital malformations manifesting as multi-organ phenotypes, affecting these related organs 1
A oligomer toxicity studies in primary cortical neuron cultures further supported these findings
Mass spectrometric analysis showed that copper ionophore treatment led to iron-sulfur cluster protein loss and subsequent proteotoxic stress in an FDX1-dependent manner, further emphasizing the interaction between FDX1, protein lipoylation machinery, and copper toxicity [3]
