ppat.1008014.g012.tif (180.55 kB)
Proposed mechanism of ETX induced transcytosis.
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posted on 2019-11-08, 18:34 authored by Jennifer R. Linden, Claudia Flores, Eric F. Schmidt, Francisco A. Uzal, Adam O. Michel, Marissa Valenzuela, Sebastian Dobrow, Timothy Vartanian(1) ETX binds to MAL and oligomerizes, (2) causing recruitment of CAV1. (3) Recruitment of CAV1 results in increased caveolae formation and internalization and is dependent on dynamin. (4) Internalized caveolae, containing various blood-borne material, rapidly fuse with EEA1+ early endosomes, which traffic contents to RAB7+ late endosomes, (5) ultimately forming MVB. We propose that MVB then fuse with the basal membrane of the endothelial cells, releasing their contents into the brain parenchyma.
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RABMAL Clostridium perfringens epsilon toxinClostridium perfringens epsilon toxinendosomeEEAInternalized caveolae fuselipid raft-dependent vacuolation60 kDA serum albumin155 kDA IgGmultivesicular bodies fuse basallyCNS microvasculaturecaveolae-dependent transcytosisETX causes blood brain barrier70 kDa dextranETX causes BBB permeability376 Da fluorescein saltETX bindingmultivesicular bodiesblood brain barrier permeabilityETX-induced BBB permeabilityexhibit ETX-induced BBB permeability
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