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Mechanistically, SSBP1 interacted with p53 and promoted DNA-PK-dependent phosphorylation of p53 at S15 to facilitate the nuclear accumulation of p53, which ultimately inhibited the transcription of SLC7A11 during ferroptosis in high fructose-treated glomerular podocytes (Fig

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Recent estimates suggest that up to 2% of children in the United States are affected by an ASD