Structural and functional differences between decay-accelerating factor and red cell acetylcholinesterase.

摘要: The abnormal erythrocytes in paroxysmal nocturnal hemoglobinuria, both PNH II (the moderately cells) and III markedly cells), lack acetylcholinesterase (AChE) activity decay-accelerating factor (DAF) activity. Both of these activities are found on glycoprotein molecules with a molecular weight about 70 Kd. To demonstrate that two fact different proteins, we have shown binding to normal red cells antibody DAF does not inhibit the subsequent monoclonal AChE nor Inhibition by polyclonal increases susceptibility lysis complement but inhibition not. rate decay C3 convertase complex classical pathway activation was inhibited added fluid phase AChE. When exhaustively immunoprecipitated from solution erythrocyte membrane remained vice versa. These studies indicate decay- accelerating which lacking erythrocytes.