ArticleProceedings of the National Academy of Sciences of the United States of America1994
Prion isolate specified allotypic interactions between the cellular and scrapie prion proteins in congenic and transgenic mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 153 citations in OpenAlex.
- Molecular signatures in prion disease: altered death receptor pathways in a mouse model.Journal of translational medicine · 2024Article
- How an Infection of Sheep Revealed Prion Mechanisms in Alzheimer's Disease and Other Neurodegenerative Disorders.International journal of molecular sciences · 2021Review
- Chronic Wasting Disease In Cervids: Prevalence, Impact And Management Strategies.Veterinary medicine (Auckland, N.Z.) · 2019Article
- A novel vector for transgenesis in the rat CNS.Acta neuropathologica communications · 2017Article
- Neurodegenerative Disease Transmission and Transgenesis in Mice.Cold Spring Harbor perspectives in biology · 2017Review
- Strains of Pathological Protein Aggregates in Neurodegenerative Diseases.Discoveries (Craiova, Romania) · 2017Review
- Bioassays and Inactivation of Prions.Cold Spring Harbor perspectives in biology · 2017Review
- Tau prions from Alzheimer's disease and chronic traumatic encephalopathy patients propagate in cultured cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Towards authentic transgenic mouse models of heritable PrP prion diseases.Acta neuropathologica · 2016Article
- Optimization of Aryl Amides that Extend Survival in Prion-Infected Mice.The Journal of pharmacology and experimental therapeutics · 2016Article
- A Common Phenotype Polymorphism in Mammalian Brains Defined by Concomitant Production of Prolactin and Growth Hormone.PloS one · 2016Article
- Prion Infectivity Plateaus and Conversion to Symptomatic Disease Originate from Falling Precursor Levels and Increased Levels of Oligomeric PrPSc Species.Journal of virology · 2015Article
- Deer Prion Proteins Modulate the Emergence and Adaptation of Chronic Wasting Disease Strains.Journal of virology · 2015Article
- Different 2-Aminothiazole Therapeutics Produce Distinct Patterns of Scrapie Prion Neuropathology in Mouse Brains.The Journal of pharmacology and experimental therapeutics · 2015Article
- Octarepeat region flexibility impacts prion function, endoproteolysis and disease manifestation.EMBO molecular medicine · 2015Article
- Evaluation of infective property of recombinant prion protein amyloids in cultured cells overexpressing cellular prion protein.Journal of Korean medical science · 2014Article
- Mouse models for studying the formation and propagation of prions.The Journal of biological chemistry · 2014Review
- Evidence that bank vole PrP is a universal acceptor for prions.PLoS pathogens · 2014Article
- Prion disease tempo determined by host-dependent substrate reduction.The Journal of clinical investigation · 2014Article
- Biaryl amides and hydrazones as therapeutics for prion disease in transgenic mice.The Journal of pharmacology and experimental therapeutics · 2013Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Different prion isolates, often referred to as "strains," present an enigma because considerable evidence argues that prions are devoid of nucleic acid. To investigate prion diversity, we inoculated three "strains" of prions into congenic and transgenic mice harboring variable numbers of two different alleles, designated a and b, of the prion protein (PrP) structural gene, Prn-p. The length of the incubation time was inversely related to the number of Prn-p(a) genes in mice inoculated with the Rocky Mountain Laboratory (RML) prion strain. Results with mice lacking this locus (Prn-p0/0) and transgenic mice argue that long incubation times are not a dominant trait as thought for many years, but rather they are due to reduced levels of the substrate PrPC-A (cellular isoform of PrP, allotype A) in (Prn-p(a) x Prn-pb)F1 mice. In contrast, the Prn-p(a) gene extended incubation times in mice inoculated with the 87V and 22A prion strains, whereas the Prn-pb gene was permissive. Experiments with the 87V isolate suggest that a genetic locus distinct from Prn-p controls deposition of the scrapie isoform of PrP (PrPSc) and attendant neuropathology. Each prion isolate produced distinguishable patterns of PrPSc accumulation in brain; of note, the patterns in Prn-p(a) and Prn-pb congenic mice inoculated with RML prions were more different than those in congenic Prn-pb mice with RML or 22A prions. Our results suggest that scrapie "strain-specific" incubation times can be explained by differences in the relative efficiency of allotypic interactions that lead to conversion of PrPC into PrPSc.
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