ArticleMolecular neurodegeneration2008
Prion protein lacks robust cytoprotective activity in cultured cells.
Article in Molecular neurodegeneration, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Expression of the Prion Protein Family Member Shadoo Causes Drug Hypersensitivity That Is Diminished by the Coexpression of the Wild Type Prion Protein.The Journal of biological chemistry · 2016Article
- Prion protein (PrP) gene-knockout cell lines: insight into functions of the PrP.Frontiers in cell and developmental biology · 2014Review
- Characterizing affinity epitopes between prion protein and β-amyloid using an epitope mapping immunoassay.Experimental & molecular medicine · 2013Article
- A genome-wide survey for prion-regulated miRNAs associated with cholesterol homeostasis.BMC genomics · 2012Article
- The N-terminal, polybasic region is critical for prion protein neuroprotective activity.PloS one · 2011Article
- Expression of prion protein in mouse erythroid progenitors and differentiating murine erythroleukemia cells.PloS one · 2011Article
- Prion neurotoxicity: insights from prion protein mutants.Current issues in molecular biology · 2010Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe physiological function of the cellular prion protein (PrPC) remains unknown. However, PrPC has been reported to possess a cytoprotective activity that prevents death of neurons and other cells after a toxic stimulus. To explore this effect further, we attempted to reproduce several of the assays in which a protective activity of PrP had been previously demonstrated in mammalian cells.
resultsIn the first set of experiments, we found that PrP over-expression had a minimal effect on the death of MCF-7 breast carcinoma cells treated with TNF-alpha and Prn-p0/0 immortalized hippocampal neurons (HpL3-4 cells) subjected to serum deprivation. In the second set of assays, we observed only a small difference in viability between cerebellar granule neurons cultured from PrP-null and control mice in response to activation of endogenous or exogenous Bax.
conclusionTaken together, our results suggest either that cytoprotection is not a physiologically relevant activity of PrPC, or that PrPC-dependent protective pathways operative in vivo are not adequately modeled by these cell culture systems. We suggest that cell systems capable of mimicking the neurotoxic effects produced in transgenic mice by N-terminally deleted forms of PrP or Doppel may represent more useful tools for analyzing the cytoprotective function of PrPC.
Identifiers
What OpenQuestion holds
Registered trials
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.