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This imbalance is marked by Drp1 hyperphosphorylation at Ser616, which amplifies fission activity, whereas suppressed MFN2 expression and aberrant OPA1 processing impair fusion, resulting in widespread mitochondrial fragmentation (Massaad and Klann, 2011
Recently, we reported a role for GPx1 in the migratory activity of triple-negative breast cancer (TNBC) cells, including MDA-MB-231 cells 55
Schedule uncertainty: Senolytic dosing is normally pulsed/intermittent, so a continuous daily schedule has no validated safety basis
Via 4E-BP, mTORC1 signaling regulates mitochondrial biogenesis as well [3]
