The effect of the calmodulin antagonist N-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamide (W-13) on the endosomal system of Madin-Darby canine kidney cells was assessed. W-13 inhibited receptor-mediated IgA transcytosis, recycling of transferrin, and caused all material endocytosed from both surfaces of the cell to be delivered to exceptionally large, novel endosomal structures, which appear to be derived from early endosomes. Treatment with other calmodulin antagonists similarly inhibited transcytosis and caused large endosomes to form. These observations raise the possibility that calmodulin may be involved in regulating membrane trafficking through the endosomes of polarized epithelial cells.
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