Moss J, Garrison S, Fishman P H, Richardson S H
J Clin Invest. 1979 Aug;64(2):381-4. doi: 10.1172/JCI109472.
Chemically transformed mouse fibroblasts did not raise their cyclic AMP level in response to Escherichia coli heat-labile enterotoxin. These fibroblasts did, however, incorporate exogenous mono-, di-, and trisialogangliosides. After the uptake of monosialoganglioside galactosyl-N-acetylgalactosaminyl-[N-acetylneuraminyl]-galactosylglucosylceramide (GM1), the cells responded to E. coli heat-labile enterotoxin. The di- and trisialogangliosides were considerably less effective. GM1, the putative cholera toxin (choleragen) receptor, has been implicated previously as the receptor for E. coli heat-labile enterotoxin based on the ability of the free ganglioside to inhibit the effects of toxin. This investigation establishes that the ganglioside, when incorporated into fibroblasts, serves a functional role in mediating the responsiveness to the toxin.
化学转化的小鼠成纤维细胞对大肠杆菌不耐热肠毒素无反应，其环磷酸腺苷水平不会升高。然而，这些成纤维细胞能够摄取外源性单唾液酸、二唾液酸和三唾液酸神经节苷脂。摄取单唾液酸神经节苷脂半乳糖基-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）后，细胞对大肠杆菌不耐热肠毒素产生反应。二唾液酸和三唾液酸神经节苷脂的效果则要差得多。GM1是公认的霍乱毒素受体，此前基于游离神经节苷脂抑制毒素作用的能力，它被认为也是大肠杆菌不耐热肠毒素的受体。本研究证实，当神经节苷脂掺入成纤维细胞时，它在介导细胞对毒素的反应中发挥功能性作用。
