Gangliosides sensitize unresponsive fibroblasts to Escherichia coli heat-labile enterotoxin.
Open Access
- 1 August 1979
- journal article
- research article
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 64 (2), 381-384
- https://doi.org/10.1172/jci109472
Abstract
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.This publication has 28 references indexed in Scilit:
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