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129/Ola mice carrying a null mutation in PrP that abolishes mRNA production are developmentally normal.

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TLDR
The use of a different targeting strategy is reported, to produce inbred mice with a complete absence of both PrP protein and mRNA sequences, which are being used in experiments designed to address the role of PrP in the pathogenesis of scrapie and the replication of infectivity.
Abstract
The neural membrane glycoprotein PrP is implicated in the pathogenesis of the transmissible spongiform encephalopathies; however, the normal function of PrP and its precise role in disease are not understood. Recently, gene targeting has been used to produce mice withneo/PrP fusion transcripts, but no detectable PrP protein in the brain (1). Here we report the use of a different targeting strategy, to produce inbred mice with a complete absence of both PrP protein and mRNA sequences. At 7 mo of age, these mice show no overt phenotypic abnormalities despite the normal high levels of expression of PrP during mouse development. The mice are being used in experiments designed to address the role of PrP in the pathogenesis of scrapie and the replication of infectivity.

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Citations
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Journal ArticleDOI

Cell surface expression of the prion protein in yeast does not alter copper utilization phenotypes

TL;DR: This report modified the PrP signal peptide by replacing its hydrophobic core with the signal sequence from the yeast protein dipeptidyl aminopeptidase B, so that the resulting protein was targeted cotranslationally to the secretory pathway when synthesized in yeast.
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Cellular prion protein prevents brain damage after encephalomyocarditis virus infection in mice

TL;DR: PrPC may play certain roles in the induction of inflammation and inhibition of apoptosis in vivo in mice infected with encephalomyocarditis virus B variant.
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Copper is toxic to PrP-ablated mice and exacerbates disease in a mouse model of E200K genetic prion disease.

TL;DR: It is shown that fibroblasts generated from both PrP-ablated mice and TgMHu2ME199K, a transgenic mouse line mimicking E200KCJD, were significantly more sensitive to copper toxicity than wt fibroBlasts, consistent with the hypothesis that a functional PrP(C) is required to protect cells from high levels of copper.
Journal ArticleDOI

Prion-associated increases in Src-family kinases.

TL;DR: Identification of similar elevations in cell culture and animal model systems suggests the elevations are a specific response to the presence of the disease-associated conformer.
Journal ArticleDOI

Lack of influence of prion protein gene expression on kainate-induced seizures in mice: studies using congenic, coisogenic and transgenic strains

TL;DR: The role of PrP in kainic acid (KA)-induced seizure sensitivity is investigated, using three types of mice and, in contrast to previous published results, Prnp-/- mice on the C57BL/10SnJ background had a significant decrease in KA-induced seizure susceptibility.
References
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Journal ArticleDOI

Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction

TL;DR: A new method of total RNA isolation by a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture is described, providing a pure preparation of undegraded RNA in high yield and can be completed within 4 h.
Journal ArticleDOI

Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours

TL;DR: Observations indicate that a normal p53 gene is dispensable for embryonic development, that its absence predisposes the animal to neoplastic disease, and that an oncogenic mutant form of p53 is not obligatory for the genesis of many types of tumours.
Journal ArticleDOI

Site-directed mutagenesis by gene targeting in mouse embryo-derived stem cells.

TL;DR: This work mutated, by gene targeting, the endogenous hypoxanthine phosphoribosyl transferase (HPRT) gene in mouse embryo-derived stem (ES) cells and compared the gene-targeting efficiencies of two classes of neor-Hprt recombinant vectors.
Journal ArticleDOI

Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC gene.

TL;DR: In this paper, a mouse lineage that exhibits an autosomal dominantly inherited predisposition to multiple intestinal neoplasia (Min) was described and linkage analysis showed that the murine homolog of the APC gene (mApc) was tightly linked to the Min locus.
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