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This research article investigates the effects of a partial deletion of the carboxyl-terminal signal sequence of the cellular prion protein (PrPC) on its expression and degradation. The study found that the resulting KIBVPrP248 mouse model exhibited significantly reduced PrPC levels and resistance to prion infection due to enhanced degradation via the endoplasmic reticulum-associated degradation pathway. The findings highlight the critical role of the C-terminal signal sequence in PrPC biogenesis and its im

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