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Unlike apoptosis, its execution is independent of caspases and is instead driven by receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3), with mixed lineage kinase domain-like protein (MLKL) acting as the executioner by oligomerizing and forming pores in the plasma membrane, leading to its rupture (41)

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In experimental autoimmune encephalomyelitis model of MS, AMPK signaling is required for oligodendrocyte function [228]