ArticlePrion2017
Limited understanding of the functional diversity of N-linked glycans as a major gap of prion biology.
Article in Prion, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 12 citations in OpenAlex.
- Reactive Microglia and Astrocytes as Therapeutic Targets in Prion Diseases.Sub-cellular biochemistry · 2025Review
- Role of sialylation of N-linked glycans in prion pathogenesis.Cell and tissue research · 2023Review
- From Posttranslational Modifications to Disease Phenotype: A Substrate Selection Hypothesis in Neurodegenerative Diseases.International journal of molecular sciences · 2021Review
- Region-specific glial homeostatic signature in prion diseases is replaced by a uniform neuroinflammation signature, common for brain regions and prion strains with different cell tropism.Neurobiology of disease · 2020Article
- Prion protein glycans reduce intracerebral fibril formation and spongiosis in prion disease.The Journal of clinical investigation · 2020Article
- Region-Specific Sialylation Pattern of Prion Strains Provides Novel Insight into Prion Neurotropism.International journal of molecular sciences · 2020Article
- Modeling PrPFrontiers in bioengineering and biotechnology · 2020Article
- Inflammatory response of microglia to prions is controlled by sialylation of PrPScientific reports · 2018Article
- Prion replication environment defines the fate of prion strain adaptation.PLoS pathogens · 2018Article
- Analyses of N-linked glycans of PrPThe FEBS journal · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Among a broad range of hypotheses on the molecular nature of transmissible spongiform encephalopathy or scrapie agents discussed in 1960s was a hypothesis of self-replicating polysaccharides. While the studies of the past 40 years provided unambiguous proof that this is not the case, emerging evidence suggests that carbohydrates in the form of sialylated N-linked glycans, which are a constitutive part of mammalian prions or PrP
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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.