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Overexpression of thioredoxin renders embryos more resistant to oxidative stress (Kobayashi-Miura et al., 2002), whereas thioredoxin null mutants exhibit dramatically reduced proliferation of the inner cell mass resulting in lethality during the early postimplantation period (reviewed in Ufer et al., 2010)

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These observations were further corroborated by RT-PCR validation of key ATF4 target genes across all ferroptosis induction conditions, which confirmed the condition-specific upregulation pattern identified in the RNA-seq dataset (Fig