PRNP and infection: Tg(PrP∆23–31)/Prnp0/0 mice, which express PrP with a deletion of the so-called N-terminal polybasic region consisting of residues 23–31 on the background of Prnp0/0, were shown to develop disease after longer incubation times with a slower accumulation of PrPSc∆23–31 in their brains after infection with RML scrapie prions, indicating that the polybasic region is important for PrPC to convert into PrPSc after prion infection (Table 2) [70].