Moss J, Fishman P H, Richards R L, Alving C R, Vaughan M, Brady R O
Proc Natl Acad Sci U S A. 1976 Oct;73(10):3480-3. doi: 10.1073/pnas.73.10.3480.
125I-Labeled choleragen was bound to liposomes containing galactosyl-N-acetylgalactosaminyl-(N-acetylneuraminyl)-galactosylglucosylceramide (GM1), but not in large amounts to ganglioside-free liposomes nor to those containing N-acetylneuraminylgalactosylglucosylceramide (GM3), N-acetylgalactosaminyl-(N-acetylneuraminyl)-galactosylglucosylceramide (GM2), or N-acetylneuraminylgalactosyl-N-acetylgalactosaminyl-(N-acetylneuraminyl)-galactosylglucosylceramide (GD1a). Choleragen released trapped glucose only from GM1-liposomes. This choleragen-induced glucose release from GM1-liposomes was relatively rapid for the first few minutes, then continued more slowly. The amount of glucose released from liposomes in 30 min was dependent on both the GM1 content and choleragen concentration. Prior incubation of GM1-liposomes with anti-GM1 antiserum prevented the choleragen-dependent release of trapped glucose. After incubation of GM1-liposomes with choleragen, addition of anticholeragen antibodies and complement led to more extensive glucose release. Under these latter conditions a much smaller glucose release was observed also from liposomes containing GM1 or N-acetylneuraminylgalactosyl-N-acetylgalactosaminyl-(N-acetylneuraminyl)-galactosylglucosylceramide in the absence of choleragen. These releases were attributed to naturally-occurring antiganglioside antibodies in the antiserum and complement. Ganglioside-free liposomes did not release glucose in response to anticholeragen and complement. It appears that choleragen in the absence of other proteins binds specifically to liposomes containing GM1 and can induce permeability changes.
125I标记的霍乱毒素与含有半乳糖基-N-乙酰半乳糖胺基-（N-乙酰神经氨酸基）-半乳糖基葡萄糖神经酰胺（GM1）的脂质体结合，但不会大量结合到不含神经节苷脂的脂质体上，也不会大量结合到含有N-乙酰神经氨酸基半乳糖基葡萄糖神经酰胺（GM3）、N-乙酰半乳糖胺基-（N-乙酰神经氨酸基）-半乳糖基葡萄糖神经酰胺（GM2）或N-乙酰神经氨酸基半乳糖基-N-乙酰半乳糖胺基-（N-乙酰神经氨酸基）-半乳糖基葡萄糖神经酰胺（GD1a）的脂质体上。霍乱毒素仅从GM1脂质体中释放被包裹的葡萄糖。这种由霍乱毒素诱导的GM1脂质体中葡萄糖的释放最初几分钟相对较快，随后释放速度减缓。30分钟内从脂质体中释放的葡萄糖量取决于GM1含量和霍乱毒素浓度。预先用抗GM1抗血清孵育GM1脂质体可阻止霍乱毒素依赖性的被包裹葡萄糖的释放。GM1脂质体与霍乱毒素孵育后，加入抗霍乱毒素抗体和补体可导致更大量的葡萄糖释放。在这些条件下，在没有霍乱毒素的情况下，从含有GM1或N-乙酰神经氨酸基半乳糖基-N-乙酰半乳糖胺基-（N-乙酰神经氨酸基）-半乳糖基葡萄糖神经酰胺的脂质体中也观察到少量的葡萄糖释放。这些释放归因于抗血清和补体中天然存在的抗神经节苷脂抗体。不含神经节苷脂的脂质体不会因抗霍乱毒素和补体而释放葡萄糖。看来在没有其他蛋白质的情况下，霍乱毒素能特异性地结合含有GM1的脂质体并能诱导通透性变化。
