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. 2004 Feb;78(4):2088–2099. doi: 10.1128/JVI.78.4.2088-2099.2004

FIG. 5.

FIG. 5.

Aberrant HuPrP(P102L) conformers present in the brains of GSS patients and GSS-inoculated Tg mice (A to D) are indistinguishable from those that progressively accumulate in spontaneously ill chimeric Tg(MHu2M,P102L) mice (E to H). Samples were developed using the 3F4 monoclonal antibody. The apparent molecular weights of migrated fragments are shown in thousands. The presence of a 22-kDa to 24-kDa PrP fragment specific to GSS prions is indicated by the arrowheads. (A to D) Brain homogenates from spontaneously ill Tg(MHu2M,P102L)69/Prnp0/0 mice (lane 2), Tg(MHu2M,P102L) mice inoculated with homogenates from GSS patients expressing either Val (lane 3) or Met (lane 4) at codon 129, and a GSS(P102L,M129) patient (lane 5). As controls, homogenates from an age-matched, healthy Tg(MHu2M)Prnp0/0 mouse (lane 1) and normal human brain (lane 6) are shown. (E to H) Brain homogenates from spontaneously ill Tg69 mice sacrificed at 50 days (lane 2), 100 days (lane 3), 200 days (lane 4), ∼360 days (lane 5), when the mice became ill, demonstrate the accumulation of PrPSc conformers that are similar to those observed in GSS patients. As a control, homogenate from a healthy, age-matched Tg(MHu2M)Prnp0/0 mouse (lane 1) is shown. Samples were untreated (A and E), precipitated with PTA (B and F), digested with PK followed by ultracentrifugation (C and G), or subjected to cold PK digestion followed by PTA precipitation (D and H).