Molecular nature of the complement lesion.
The principle molecular event leading to membrane perturbation by complement is the assembly of the terminal five serum complement components (C5b-C9) into a macromolecular C5b-9 complex on the target membrane [Müller-Eberhard, H.-J. (1975) Ann. Rev. Biochem. 44, 697--723]. The present communication reports on the ability of purified C5b-9 complexes isolated from target membranes to become reincorporated into artificial lipid vesicles. The data indicate that the complex is a vertically oriented, hollow, cylindrical macromolecule possessing lipid-binding regions that enable one terminus to penetrate into the lipid bilayer. A transmembrane pore appears to be created at the attachment site of the C5b-9 complex.
D000818:Animals; D003165:Complement System Proteins; D004910:Erythrocyte Membrane / Q000648:ultrastructure; D006801:Humans; D007122:Immunoelectrophoresis; D008563:Membrane Lipids / Q000097:blood; D008567:Membranes, Artificial; D008854:Microscopy, Electron; D012756:Sheep
D008563:Membrane Lipids; D008567:Membranes, Artificial; D003165:Complement System Proteins