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Our findings indicate that FOXO4-DRI promotes apoptosis in senescent cells by disrupting the FOXO4-P53 interaction, thereby releasing and phosphorylating P53, which then translocates to the cytoplasm
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Following hCiPSC treatment, the microbial community composition shifted towards the control state, as evidenced by significantly reduced dissimilarity to the VPA-ASD model (Figure S4B)
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