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Interaction of the lipid-tethered protein (FR-GPI) and the actin-binding transmembrane protein (FRTM-Ez-AFBD) with the actin cytoskeleton, via lipid-based transbilayer interactions or by direct actin binding, induces the formation of large receptor platforms. The lack of this interaction in the mutated receptor (FRTM-Ez-AFBD*) prevents large-scale correlation and confines the receptors within the actin meshwork.
