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Indeed, adipocyte-specific deletion of phosphatase protector 4 increases the expression of protein tyrosine phosphatase 1B (PTP1B), thereby enhancing dephosphorylation of the insulin receptor, which dampens insulin signaling, impairs adipogenesis, and alters mitochondrial oxidation [52]

Rather, Grx2 overexpression cleared mutant SOD1 in the mitochondria, resulting in decreased mitochondrial fragmentation and abolishing neuron apoptosis [27]

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