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Moreover, mitochondrial iron overload inhibits Fe-S cluster-dependent enzymes such as aconitase 2, leading to the accumulation of metabolites like succinate

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Suppressing the localized immune response that mistakenly attacks the skins pigment, allowing for a stable recovery environment

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This is evidenced by the fact that we have now identified two different classes of drug, lobeline (monoamine metabolism) and raloxifene (SERM) that clearly function through different mechanisms yet yield the same result: delayed SG disassembly, prolonged ISR activation and increased GBM cell death