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Mitochondrial fission regulator 1-like (MTFR1L) is an outer mitochondrial membrane-localized protein required for the adaptation of mitochondrial morphology and dynamics in response to metabolic changes. It regulates mitochondrial shape, acting primarily as a negative regulator of mitochondrial fusion by controlling levels of the mitochondrial inner membrane fusion protein OPA1. MTFR1L is phosphorylated by AMP-activated protein kinase (AMPK), and this phosphorylation is essential for its function in mediating stress-induced mitochondrial fragmentation. Loss of MTFR1L results in mitochondrial elongation, increased mitochondrial interconnectivity, and cellular resistance to apoptosis, revealing its central role in the balance of mitochondrial fission and fusion in both mammalian cells and murine neurons[1][2][3][4].
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