Atypical Scrapie Prions from Sheep and Lack of Disease in Transgenic Mice Overexpressing Human Prion Protein
Jonathan D.F. Wadsworth
, Susan Joiner, Jacqueline M. Linehan, Anne Balkema-Buschmann, John Spiropoulos, Marion M. Simmons, Peter C. Griffiths, Martin H. Groschup, James Hope, Sebastian Brandner, Emmanuel A. Asante, and John Collinge
Author affiliations: University College London, London, UK (J.D.F Wadsworth, S. Joiner, J.M. Linehan, S. Brandner, E.A. Asante, J. Collinge); Federal Research Institute for Animal Health, Greifswald-Insel Riems, Germany (A. Anne Balkema-Buschmann, M.H. Groschup); Animal Health and Veterinary Laboratories Agency, Addlestone, UK (J. Spiropoulos, M.M. Simmons, P.C. Griffiths, J. Hope)
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Figure 3
Figure 3. . Ovine bovine spongiform encephalopathy (BSE) prion transmission to a 129MM Tg35c mouse. Panel A shows immunoblot detection of disease-related prion protein (PrPSc) in 10 μL of proteinase K (PK)–digested 10% (w/v) brain homogenates from ovine BSE (SE 1929/0877) (lane 1) and secondary passage ovine BSE (SE1945/0032) (lane 2) using monoclonal antibody ICSM35 against prion protein (PrP). Panel B shows type 4 PrPSc in 1 μL of PK-digested 10% (w/v) vCJD brain homogenate (lane 1) in comparison to PrPSc in 20 μL of PK-digested 10% (w/v) brain homogenate from a 129MMTg35c mouse with subclinical prion infection that was culled 661 days after inoculation with secondary passage ovine BSE inoculum SE1945/0032 (lane 2). Panel C shows abnormal PrP immunoreactivity stained with monoclonal antibody ICSM35 against PrP in the corpus callosum of the ovine BSE–affected 129MM Tg35c mouse brain. Scale bar indicates 165 μm.
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