Lorand L, Barnes N, Bruner-Lorand J A, Hawkins M, Michalska M
Biochemistry. 1987 Jan 13;26(1):308-13. doi: 10.1021/bi00375a043.
Treatment of human erythrocytes with Ca2+, in the presence of ionophore A23187, causes the formation of high molecular weight (greater than 10(6)) membrane protein polymers. This phenomenon, known to involve cross-linking of essentially all of the band 4.1 and 2.1 (ankyrin) proteins, as well as some spectrin, band 3, and hemoglobin molecules, could be prevented by preincubating the cells with a noncompetitive inhibitor of intrinsic transglutaminase, 2-[3-(diallylamino)propionyl]benzothiophene, at concentrations of about (3-6) X 10(-4) M. The compound also eliminated the proteolytic breakdown of the two major transmembrane proteins band 3 and glycophorin, which would otherwise occur during the Ca2+ loading of fresh human red cells. In addition, the inhibitor effectively blocked the formation of a cross-linked protein polymer in thrombin-activated human platelets.
在离子载体A23187存在的情况下，用Ca2+处理人红细胞会导致形成高分子量（大于10(6)）的膜蛋白聚合物。已知这种现象涉及基本上所有的4.1带和2.1带（锚蛋白）蛋白以及一些血影蛋白、3带和血红蛋白分子的交联，通过用浓度约为(3 - 6)×10(-4) M的内在转谷氨酰胺酶的非竞争性抑制剂2-[3-(二烯丙基氨基)丙酰基]苯并噻吩对细胞进行预孵育，可以防止这种现象。该化合物还消除了两种主要跨膜蛋白3带和血型糖蛋白的蛋白水解降解，否则在新鲜人红细胞的Ca2+加载过程中会发生这种降解。此外，该抑制剂有效地阻断了凝血酶激活的人血小板中交联蛋白聚合物的形成。
