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proposed that excessive mitochondrial division in pluripotent stem cells (PSCs) bridges driving mitochondrial dynamics and Ca 2+ homeostasis by increasing cytoplasmic Ca 2+ entry and CaMKII activity, leading to ubiquitin-mediated proteasomal degradation of β-Catenin, suggesting that the balance between mitochondrial fusion and division is critical for maintaining Ca 2+ homeostasis (82)
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