Abstract
Many physiological ligands, toxins, and viruses enter mammalian cells through receptor-mediated endocytosis. After entry in coated vesicles, they appear in uncoated vesicles called endosomes, which serve as intermediates in the transfer of ligands from the cell surface to lysosomes. Evidence suggests that once internalized, the toxic subunit of diphtheria toxin and the nucleic acid of several animal viruses gain access to the cytosol of host cells through an acidic intracellular compartment(s). A mutation conferring resistance to diphtheria toxin that also confers resistance to these viruses could indicate a defect in the acidification of this compartment(s). In this report, we discuss our recent evidence that one class of “cross-resistant” mutants from CHO-K1 cells have such a defect.
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Nygård, O., Westermann, P. (1983). Defective Endosome Acidification in Mammalian Cell Mutants “Cross-Resistant” to Certain Toxins and Viruses. In: Abraham, A.K., Eikhom, T.S., Pryme, I.F. (eds) Protein Synthesis. Humana Press. https://doi.org/10.1007/978-1-4612-5310-5_18
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DOI: https://doi.org/10.1007/978-1-4612-5310-5_18
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