PRNP and prion disease: These results suggest that residues 91–106 of PrPC are essential for RML, 22L and FK-1 prions but not for BSE prions, to induce the conversion of PrPC into PrPSc and eventually cause prion disease in mice, although the lower expression of PrP∆91–106 in the brain might be partly responsible for the longer incubation times in BSE-infected Tg(PrP∆91–106)/Prnp0/0 mice.