ReviewViruses2012
Cellular prion protein: from physiology to pathology.
Review in Viruses, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
- Re-evaluation of the relationship between PrPc expression and patient prognosis in primary esophageal squamous cell carcinoma and primary hepatocellular carcinoma.Scientific reports · 2024Article
- Differential expression of cellular prion protein (PrPJournal of neurovirology · 2024Article
- Molecular signatures in prion disease: altered death receptor pathways in a mouse model.Journal of translational medicine · 2024Article
- Prion Protein: The Molecule of Many Forms and Faces.International journal of molecular sciences · 2022Review
- Transgenic Overexpression of the Disordered Prion Protein N1 Fragment in Mice Does Not Protect Against Neurodegenerative Diseases Due to Impaired ER Translocation.Molecular neurobiology · 2020Article
- Intrinsic toxicity of the cellular prion protein is regulated by its conserved central region.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Genetic PrP Prion Diseases.Cold Spring Harbor perspectives in biology · 2018Review
- Prion disease.Handbook of clinical neurology · 2018Review
- The biological function of the cellular prion protein: an update.BMC biology · 2017Review
- Genetic prion disease: Experience of a rapidly progressive dementia center in the United States and a review of the literature.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2017Review
- The Biological Function of the Prion Protein: A Cell Surface Scaffold of Signaling Modules.Frontiers in molecular neuroscience · 2017Article
- Hypoxia-induced expression of cellular prion protein improves the therapeutic potential of mesenchymal stem cells.Cell death & disease · 2016Article
- Prion Protein and Stage Specific Embryo Antigen 1 as Selection Markers to Enrich the Fraction of Murine Embryonic Stem Cell-Derived Cardiomyocytes.Yonago acta medica · 2016Article
- Article
- Biochemical insight into the prion protein family.Frontiers in cell and developmental biology · 2015Review
- Plasma soluble prion protein, a potential biomarker for sport-related concussions: a pilot study.PloS one · 2015Article
- Therapeutic molecules and endogenous ligands regulate the interaction between brain cellular prion protein (PrPC) and metabotropic glutamate receptor 5 (mGluR5).The Journal of biological chemistry · 2014Article
- Prion (PrPC) expression in ovine uteroplacental tissues increases after estrogen treatment of ovariectomized ewes and during early pregnancy.Reproduction (Cambridge, England) · 2014Article
- Alzheimer's disease and prion protein.Intractable & rare diseases research · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human cellular prion protein (PrP(C)) is a glycosylphosphatidylinositol (GPI) anchored membrane glycoprotein with two N-glycosylation sites at residues 181 and 197. This protein migrates in several bands by Western blot analysis (WB). Interestingly, PNGase F treatment of human brain homogenates prior to the WB, which is known to remove the N-glycosylations, unexpectedly gives rise to two dominant bands, which are now known as C-terminal (C1) and N-terminal (N1) fragments. This resembles the β-amyloid precursor protein (APP) in Alzheimer disease (AD), which can be physiologically processed by α-, β-, and γ-secretases. The processing of APP has been extensively studied, while the identity of the cellular proteases involved in the proteolysis of PrP(C) and their possible role in prion biology has remained limited and controversial. Nevertheless, there is a strong correlation between the neurotoxicity caused by prion proteins and the blockade of their normal proteolysis. For example, expression of non-cleavable PrP(C) mutants in transgenic mice generates neurotoxicity, even in the absence of infectious prions, suggesting that PrP(C) proteolysis is physiologically and pathologically important. As many mouse models of prion diseases have recently been developed and the knowledge about the proteases responsible for the PrP(C) proteolysis is accumulating, we examine the historical experimental evidence and highlight recent studies that shed new light on this issue.
Indexed as
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.