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Preclinical data suggest potential neuroprotective mechanisms tied to mitochondrial support and anti-apoptotic signaling, hinting at experimental relevance in brain injury and age-related degeneration[1][11]

Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours

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mTORC2 also phosphorylates SGK-1 at Ser422, leading to inhibitory phosphorylation of FoxO3 and other activators of autophagy, such as VDAC1 and ULK1 [296]