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Their work showed that restoring MST1 expression activates p53, which subsequently phosphorylates Drp1 at Ser616 to facilitate mitochondrial fission while concurrently suppresses Parkin transcription (61)
This downregulation leads to the accumulation of the intermediate 3-hydroxy-lanost-8-en-32-al, a known translational repressor of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR)
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