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Using a multifaceted approach, we demonstrate that reducing GSH biosynthesis led to acute degradation of RUNX2, impaired osteoblast differentiation, and reduced bone formation

A recent study found that SAT1 (the gene encodes SSAT) is a transcriptional target of p53 and participates in p53-mediated ferroptosis (Ou et al., 2016)

Generally, N -acetylcysteine, the standard antidote for APAP toxicity, is sufficient treatment because it replenishes GSH and also directly detoxifies NAPQI

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