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    A single amino acid alteration (101L) introduced into murine PrP dramatically alters incubation time of transmissible spongiform encephalopathy

    Date
    1999-12-01
    Author
    Manson, Jean C.
    Jamieson, Elizabeth
    Baybutt, Herbert
    Tuzi, Nadia L.
    Barron, Rona
    McConnell, Irene
    Somerville, Robert
    Ironside, James
    Will, Robert
    Sy, Man-Sun
    Melton, David W.
    Hope, James
    Bostock, Christopher
    Metadata
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    Citation
    Manson, J.C. (1999) ‘A single amino acid alteration (101l) introduced into murine PrP dramatically alters incubation time of transmissible spongiform encephalopathy’, The EMBO Journal, 18(23), pp. 6855–6864. Available at: https://doi.org/10.1093/emboj/18.23.6855.
    Abstract
    A mutation equivalent to P102L in the human PrP gene, associated with Gerstmann–Straussler syndrome (GSS), has been introduced into the murine PrP gene by gene targeting. Mice homozygous for this mutation (101LL) showed no spontaneous transmissible spongiform encephalopathy (TSE) disease, but had incubation times dramatically different from wild-type mice following inoculation with different TSE sources. Inoculation with GSS produced disease in 101LL mice in 288 days. Disease was transmitted from these mice to both wild-type (226 days) and 101LL mice (148 days). In contrast, 101LL mice infected with ME7 had prolonged incubation times (338 days) compared with wild-type mice (161 days). The 101L mutation does not, therefore, produce any spontaneous genetic disease in mice but significantly alters the incubation time of TSE infection. Additionally, a rapid TSE transmission was demonstrated despite extremely low levels of disease-associated PrP.
    URI
    https://eresearch.qmu.ac.uk/handle/20.500.12289/12729
    Official URL
    https://doi.org/10.1093/emboj/18.23.6855
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    • Dietetics, Nutrition and Biological Sciences

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