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Schematic summary of proposed model. The ABD of FLN interacts with F-actin and ASB2α. ASB2α targets lysine residues within FLN CH1 domain, and mutations in CH1 render FLN ASB2α-resistant. FLN bound to F-actin is protected from ASB2α-mediated degradation and regulates cell spreading. Upon dissociation from F-actin, lysine residues within the CH1 are exposed and available for polyubiquitination leading to subsequent proteasomal degradation.
