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• W2074888950 endingPage "4120" @default.
• W2074888950 startingPage "4107" @default.
• W2074888950 abstract "The flow of material from peripheral, early endosomes to late endosomes requires microtubules and is thought to be facilitated by the minus end-directed motor cytoplasmic dynein and its activator dynactin. The microtubule-binding protein CLIP-170 may also play a role by providing an early link to endosomes. Here, we show that perturbation of dynactin function in vivo affects endosome dynamics and trafficking. Endosome movement, which is normally bidirectional, is completely inhibited. Receptor-mediated uptake and recycling occur normally, but cells are less susceptible to infection by enveloped viruses that require delivery to late endosomes, and they show reduced accumulation of lysosomally targeted probes. Dynactin colocalizes at microtubule plus ends with CLIP-170 in a way that depends on CLIP-170’s putative cargo-binding domain. Overexpression studies using p150 Glued , the microtubule-binding subunit of dynactin, and mutant and wild-type forms of CLIP-170 indicate that CLIP-170 recruits dynactin to microtubule ends. These data suggest a new model for the formation of motile complexes of endosomes and microtubules early in the endocytic pathway." @default.
• W2074888950 created "2016-06-24" @default.
• W2074888950 creator A5003988078 @default.
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• W2074888950 date "1999-12-01" @default.
• W2074888950 modified "2023-10-01" @default.
• W2074888950 title "Role of Dynactin in Endocytic Traffic: Effects of Dynamitin Overexpression and Colocalization with CLIP-170" @default.
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• W2074888950 doi "https://doi.org/10.1091/mbc.10.12.4107" @default.
• W2074888950 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/25746" @default.
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• W2074888950 hasPublicationYear "1999" @default.
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