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@ARTICLE{Fehlinger:139807,
      author       = {Fehlinger, Andrea and Wolf, Hanna and Hossinger, André and
                      Dürnberger, Yvonne and Pleschka, Catharina and Riemschoß,
                      Katrin and Liu, Shu and Bester, Romina and Paulsen, Lydia
                      and Priola, Suzette A and Groschup, Martin H and Schätzl,
                      Hermann M and Vorberg, Ina M},
      title        = {{P}rion strains depend on different endocytic routes for
                      productive infection.},
      journal      = {Scientific reports},
      volume       = {7},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DZNE-2020-06129},
      pages        = {6923},
      year         = {2017},
      abstract     = {Prions are unconventional agents composed of misfolded
                      prion protein that cause fatal neurodegenerative diseases in
                      mammals. Prion strains induce specific neuropathological
                      changes in selected brain areas. The mechanism of
                      strain-specific cell tropism is unknown. We hypothesised
                      that prion strains rely on different endocytic routes to
                      invade and replicate within their target cells. Using prion
                      permissive cells, we determined how impairment of
                      endocytosis affects productive infection by prion strains
                      22L and RML. We demonstrate that early and late stages of
                      prion infection are differentially sensitive to perturbation
                      of clathrin- and caveolin-mediated endocytosis. Manipulation
                      of canonical endocytic pathways only slightly influenced
                      prion uptake. However, blocking the same routes had drastic
                      strain-specific consequences on the establishment of
                      infection. Our data argue that prion strains use different
                      endocytic pathways for infection and suggest that cell
                      type-dependent differences in prion uptake could contribute
                      to host cell tropism.},
      keywords     = {Animals / Biological Transport / Caveolin 1: metabolism /
                      Cell Line / Cell Membrane: metabolism / Endocytosis / Mice /
                      PrPSc Proteins: metabolism / PrPSc Proteins: pathogenicity /
                      Prion Diseases: metabolism / Cav1 protein, mouse (NLM
                      Chemicals) / Caveolin 1 (NLM Chemicals) / PrPSc Proteins
                      (NLM Chemicals)},
      cin          = {AG Vorberg},
      ddc          = {600},
      cid          = {I:(DE-2719)1013004},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28761068},
      pmc          = {pmc:PMC5537368},
      doi          = {10.1038/s41598-017-07260-2},
      url          = {https://pub.dzne.de/record/139807},
}