Richards R L, Moss J, Alving C R, Fishman P H, Brady R O
Proc Natl Acad Sci U S A. 1979 Apr;76(4):1673-6. doi: 10.1073/pnas.76.4.1673.
Choleragen (cholera toxin) agglutinated erythrocytes and liposomes containing the toxin receptor, galactosyl-N-acetylgalactosaminyl-(N-acetylneuraminyl)-galactosylglucosylceramide (ganglioside GM1). Cells that had been exposed to GM1 were agglutinated, but agglutination was not observed when cells had been exposed to other gangliosides (GM2, GM3, GD1a, GD1b). Choleragen-dependent agglutination of liposomes was slightly less specific, because liposomes containing either GM1 or GD1b, but neither GM2, GD1a, nor GM3 were agglutinated. The oligosaccharide isolated from GM1 inhibited both the agglutination of cells and liposomes containing GM1 and the binding of choleragen to liposomes containing GM1. Galactose and sialic acid were less effective inhibitors of liposomal agglutination and did not inhibit cellular agglutination or binding of choleragen to liposomes. Liposomal agglutination was dependent on choleragen concentration and occurred with the B but not the A protomer of choleragen. These results suggest that choleragen, through its binding to the oligosaccharide portion of a glycolipid, exhibits lectinlike activity, which results in agglutination of liposomes and erythrocytes.
霍乱毒素能凝集红细胞以及含有毒素受体半乳糖基-N-乙酰半乳糖胺基-（N-乙酰神经氨酸基）-半乳糖基葡糖神经酰胺（神经节苷脂GM1）的脂质体。接触过GM1的细胞会发生凝集，但接触其他神经节苷脂（GM2、GM3、GD1a、GD1b）的细胞则未观察到凝集现象。霍乱毒素依赖的脂质体凝集特异性稍低，因为含有GM1或GD1b但不含GM2、GD1a或GM3的脂质体都会发生凝集。从GM1中分离出的寡糖既能抑制含有GM1的细胞和脂质体的凝集，也能抑制霍乱毒素与含有GM1的脂质体的结合。半乳糖和唾液酸对脂质体凝集的抑制作用较弱，且不抑制细胞凝集或霍乱毒素与脂质体的结合。脂质体凝集依赖于霍乱毒素浓度，且由霍乱毒素的B亚基而非A亚基引起。这些结果表明，霍乱毒素通过与糖脂的寡糖部分结合，表现出类凝集素活性，从而导致脂质体和红细胞的凝集。
