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• W2810949311 abstract "Ebola virus (EBOV) enters host cells by macropinocytosis, a poorly understood process. Recent studies have suggested that cell factors involved in autophagy, an evolutionally conserved pathway leading to the lysosomal degradation of protein aggregates and organelles during cellular stress, also have roles in macropinocytosis. Here, we demonstrate that autophagy-associated proteins are required for trafficking of EBOV into the cell body. Depleting cells of beclin 1, autophagy-related protein 7, or microtubule-associated protein 1A/B light chain 3B (LC3B) abolished EBOV uptake, owing to a block in vesicle formation at the cell surface. Both LC3B-I and LC3B-II interacted with macropinocytic structures. Our work indicates that, although various forms of LC3B possess an inherent ability to associate with forming macropinosomes, LC3B-II is critical for internalization of macropinocytic vesicles and, therefore, EBOV from the cell surface." @default.
• W2810949311 created "2018-07-10" @default.
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• W2810949311 date "2018-06-27" @default.
• W2810949311 modified "2023-09-27" @default.
• W2810949311 title "Autophagy-Associated Proteins Control Ebola Virus Internalization Into Host Cells" @default.
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• W2810949311 doi "https://doi.org/10.1093/infdis/jiy294" @default.
• W2810949311 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6249560" @default.
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