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Adult mice with a deletion of MDM4, an MDM2 homolog and a negative regulator of p53, exhibited dilated cardiomyopathy

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This indicates that survival is critically dependent upon GSH, and therefore is not being sustained by an alternative Trx-disulfide reductase, such as by repurposing of either the mitochondrial TrxR2 or the testis-specific Tgr (TrxR3) [48, 109]

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