作者: Robert A. Spooner , Peter Watson , Daniel C. Smith , Frédéric Boal , Mohammed Amessou
DOI: 10.1042/BJ20080149
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摘要: The small-molecule inhibitor Exo2 {4-hydroxy-3-methoxy-(5,6,7,8-tetrahydrol[1]benzothieno[2,3-d]pyrimidin-4-yl)hydraz-one benzaldehyde} has been reported to disrupt the Golgi apparatus completely and stimulate Golgi–ER (endoplasmic reticulum) fusion in mammalian cells, akin well-characterized fungal toxin BFA (brefeldin A). It also that does not affect integrity of TGN (trans-Golgi network), or direct retrograde trafficking glycolipid-binding cholera from ER lumen. We have examined effects Exo2, found both compounds are indistinguishable their inhibition anterograde transport reagents significantly morphology HeLa BS-C-1 cells. However, unlike BFA, induce tubulation merging endosomal compartments. Furthermore, contrast with its on toxin, perturbs delivery Shiga ER. Together, these results suggest likely target(s) operate at level TGN, a subset early endosomes, thus provides more selective tool than for examining membrane