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These metabolic and proteomic changes collectively indicate that in ATP6AP1 KO cells show a metabolic phenotype protected from ACT-induced rerouting of carbons, suggestive that partial v-ATPase disruption appears to reduce cellular reliance on mitochondrial oxidation, enabling resistance to mitochondrial insults while limiting biosynthetic capacity

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However, scientists still do not fully understand how DSIP works in the body

p62/SQSTM1 at the interface of aging, autophagy, and disease