ArticleBMC genomics2010
Brain transcriptional stability upon prion protein-encoding gene invalidation in zygotic or adult mouse.
Article in BMC genomics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- The multiple functions of PrPJournal of molecular medicine (Berlin, Germany) · 2022Review
- Loss of prion protein control of glucose metabolism promotes neurodegeneration in model of prion diseases.PLoS pathogens · 2021Article
- The Cellular Prion Protein-ROCK Connection: Contribution to Neuronal Homeostasis and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Review
- The Prion Protein Regulates Synaptic Transmission by Controlling the Expression of Proteins Key to Synaptic Vesicle Recycling and Exocytosis.Molecular neurobiology · 2019Article
- The biological function of the cellular prion protein: an update.BMC biology · 2017Review
- Article
- Strictly co-isogenic C57BL/6J-Prnp-/- mice: A rigorous resource for prion science.The Journal of experimental medicine · 2016Article
- Mutated but Not Deleted Ovine PrP(C) N-Terminal Polybasic Region Strongly Interferes with Prion Propagation in Transgenic Mice.Journal of virology · 2016Article
- Gene expression resulting from PrPC ablation and PrPC overexpression in murine and cellular models.Molecular neurobiology · 2014Review
- The prion protein family: a view from the placenta.Frontiers in cell and developmental biology · 2014Review
- To develop with or without the prion protein.Frontiers in cell and developmental biology · 2014Review
- Prion protein and Shadoo are involved in overlapping embryonic pathways and trophoblastic development.PloS one · 2012Article
- Transcriptomic analysis brings new insight into the biological role of the prion protein during mouse embryogenesis.PloS one · 2011Article
- Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe physiological function of the prion protein remains largely elusive while its key role in prion infection has been expansively documented. To potentially assess this conundrum, we performed a comparative transcriptomic analysis of the brain of wild-type mice with that of transgenic mice invalidated at this locus either at the zygotic or at the adult stages.
resultsOnly subtle transcriptomic differences resulting from the Prnp knockout could be evidenced, beside Prnp itself, in the analyzed adult brains following microarray analysis of 24 109 mouse genes and QPCR assessment of some of the putatively marginally modulated loci. When performed at the adult stage, neuronal Prnp disruption appeared to sequentially induce a response to an oxidative stress and a remodeling of the nervous system. However, these events involved only a limited number of genes, expression levels of which were only slightly modified and not always confirmed by RT-qPCR. If not, the qPCR obtained data suggested even less pronounced differences.
conclusionsThese results suggest that the physiological function of PrP is redundant at the adult stage or important for only a small subset of the brain cell population under classical breeding conditions. Following its early reported embryonic developmental regulation, this lack of response could also imply that PrP has a more detrimental role during mouse embryogenesis and that potential transient compensatory mechanisms have to be searched for at the time this locus becomes transcriptionally activated.
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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.