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10.1016/j.cbi.2021.109402 88 ImaiS.GuarenteL
doi: 10.1038/s41586-020-2456-9 231 Robledinos-AntnN.Fernndez-GinsR.MandaG.CuadradoA
In the absence of other key acetylation sites in the DNA-binding domain, the absence of K98 acetylation will prevent p53 from mediating ferroptosis through acetylated targets and effectively inhibiting tumor growth[127]
[1] In an average adult, only a small amount (approximately 10% of a therapeutic paracetamol dose) of NAPQI is produced, which is inactivated by conjugation with glutathione (GSH)
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