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Its causes are poorly understood and therapies are largely ineffective

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Research shows that in senescent cells, p53 levels are maintained low through ubiquitination while its pro-apoptotic activity is repressed through nuclear segregation by FOXO4. The peptide's competitive inhibition restores p53 activity by promoting nuclear exclusion, allowing p53 to execute its pro-apoptotic program and eliminate senescent cells through targeted pathway activation

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