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Once this interaction is disrupted: p53 is released from the nucleus Cellular self-destruction pathways are activated Senescent cells undergo apoptosis This selective mechanism has made FOXO4-DRI one of the most studied senolytic peptides in modern aging research
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Upregulation of GAT3 was also observed in SZ DLPFC and considered to be the result of a compensative mechanism activated in response to GAT1 deficit [161]
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