ArticleThe Journal of biological chemistry2008
Dominant-negative effects of the N-terminal half of prion protein on neurotoxicity of prion protein-like protein/doppel in mice.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Strain-Dependent Prion Infection in Mice Expressing Prion Protein with Deletion of Central Residues 91-106.International journal of molecular sciences · 2020Article
- Protective anti-prion antibodies in human immunoglobulin repertoires.EMBO molecular medicine · 2020Article
- Prion protein signaling induces M2 macrophage polarization and protects from lethal influenza infection in mice.PLoS pathogens · 2020Article
- The N-Terminal Polybasic Region of Prion Protein Is Crucial in Prion Pathogenesis Independently of the Octapeptide Repeat Region.Molecular neurobiology · 2020Article
- Prion protein protects mice from lethal infection with influenza A viruses.PLoS pathogens · 2018Article
- Prion Protein Devoid of the Octapeptide Repeat Region Delays Bovine Spongiform Encephalopathy Pathogenesis in Mice.Journal of virology · 2018Article
- Cyclin-dependent kinase 5 phosphorylation of familial prion protein mutants exacerbates conversion into amyloid structure.The Journal of biological chemistry · 2015Article
- Ataxia with cerebellar lesions in mice expressing chimeric PrP-Dpl protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Critical significance of the region between Helix 1 and 2 for efficient dominant-negative inhibition by conversion-incompetent prion protein.PLoS pathogens · 2013Article
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- A nine amino acid domain is essential for mutant prion protein toxicity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- The N-terminal, polybasic region is critical for prion protein neuroprotective activity.PloS one · 2011Article
- Prion neurotoxicity: insights from prion protein mutants.Current issues in molecular biology · 2010Review
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Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion protein-like protein/doppel is neurotoxic, causing ataxia and Purkinje cell degeneration in mice, whereas prion protein antagonizes doppel-induced neurodegeneration. Doppel is homologous to the C-terminal half of prion protein but lacks the amino acid sequences corresponding to the N-terminal half of prion protein. We show here that transgenic mice expressing a fusion protein consisting of the N-terminal half, corresponding to residues 1-124, of prion protein and doppel in neurons failed to develop any neurological signs for up to 730 days in a background devoid of prion protein. In addition, the fusion protein prolonged the onset of ataxia in mice expressing exogenous doppel. These results suggested that the N-terminal part of prion protein has a neuroprotective potential acting both cis and trans on doppel. We also show that prion protein lacking the pre-octapeptide repeat (Delta25-50) or octapeptide repeat (Delta51-90) region alone could not impair the antagonistic function against doppel.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.