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Accumulated p53 is stabilized and activated through posttranslational modifications, including methylation, phosphorylation and acetylation, 53 which regulate gene transcription and affect a series of signaling pathways involved in apoptosis, cell cycle arrest, senescence, autophagy, ferroptosis, cellular metabolism and the tumor immune microenvironment (TME) 54,55,56 (Fig

In this Review, we discuss the evidence for these interacting pathways and describe how the capacity of KIT, and other receptors, to influence FcRI-dependent mast-cell-mediator release might be a function of the relative abilities of these receptors to activate these alternative pathways

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2 MASLD is primarily characterized by abnormal lipid accumulation in hepatocytes, typically presenting as simple steatosis

Many detoxifying enzymes that target the downstream products of peroxidation after ferroptosis are also activated by Nrf2