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ESCRT-III, in conjunction with associated proteins, facilitates the final split of vesicles and participates in protein deubiquitination

This dual action suggests sophisticated regulatory mechanisms for maintaining neural balance[2]

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Multiple mechanisms including loss-of-function mutations in the genes encoding NRF2 or small Mafs, oxidation or epigenetic modification of the NRF2 promoter, or changes in the other factors that modulate NRF2 (such as kinases, phosphatases, or DNA binding proteins) have been suggested to contribute to the suppression of NRF2 activity during ageing