Moreover, cofilin activates phagocytosis by advancing the remodeling of actin filaments (i.e., existing filaments disassemble and new filaments assemble in a new configuration), causing filopodia/lamellipodia to protrude, and furthermore, Galectin-3 (formally named MAC-2) activates phagocytosis by enhancing K-Ras.GTP/PI3K signaling that leads to actin/myosin-based contraction, causing filopodia/lamellipodia to retract. We previously showed that in phagocytosis, filopodia and lamellipodia extend/engulf and then retract/internalize myelin-debris. Therefore, revealing mechanisms that control phagocytosis is vital. These devastating outcomes are largely due to inefficient removal by phagocytosis of myelin-debris by microglia. Myelin-debris so produced is harmful to repair since it impedes remyelination in MS and the regeneration of traumatized axons. Myelin surrounding central nervous system (CNS) axons breaks down in multiple sclerosis (MS) and following traumatic axonal injury. Department of Medical Neurobiology, Institute for Medical Research Israel–Canada (IMRIC), Faculty of Medicine, Hebrew University, Jerusalem, Israel.
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