ArticleThe Journal of clinical investigation2020
Posttranslational modifications define course of prion strain adaptation and disease phenotype.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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.
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Who cites it
31 citing papers in PubMed, 42 citations in OpenAlex.
- The Phenotypic Spectrum of Sporadic Creutzfeldt-Jakob Disease Cortical Subtype.Annals of neurology · 2026Article
- Article
- Discovering, Integrating, and Reinterpreting the Molecular Logic of Life: From Classical Theories of Heredity to an Extended Functional Perspective on the Central Dogma.Life (Basel, Switzerland) · 2026Review
- Knockout of P2Y12 receptor facilitates neuronal envelopment by reactive microglia and accelerates prion disease.Journal of neuroinflammation · 2025Article
- Acetylation mimetic and null mutations within the filament core of P301L tau have varied effects on susceptibility to seeding and aggregation.bioRxiv : the preprint server for biology · 2025Article
- Dissecting surveying behavior of reactive microglia under chronic neurodegeneration.bioRxiv : the preprint server for biology · 2025Article
- Downregulation of STAT3 transcription factor reverses synaptotoxic phenotype of reactive astrocytes associated with prion diseases.Acta neuropathologica communications · 2025Article
- Knockout of P2Y12 receptor facilitates microglia-neuron body-to-body interactions and accelerates prion disease.bioRxiv : the preprint server for biology · 2025Article
- Reactive Microglia and Astrocytes as Therapeutic Targets in Prion Diseases.Sub-cellular biochemistry · 2025Review
- Reactive astrocytes in prion diseases: Friend or foe?PLoS pathogens · 2024Review
- Review
- Emerging role of microglia in inter-cellular transmission of α-synuclein in Parkinson's disease.Frontiers in aging neuroscience · 2024Review
- Post-translational modifications in prion diseases.Frontiers in molecular neuroscience · 2024Review
- Multiple steps of prion strain adaptation to a new host.Frontiers in neuroscience · 2024Article
- Propagation of PrPCommunications biology · 2023Article
- Reactive astrocytes associated with prion disease impair the blood brain barrier.Neurobiology of disease · 2023Article
- Article
- Antisense oligonucleotide therapy for H3.3K27M diffuse midline glioma.Science translational medicine · 2023Article
- Role of sialylation of N-linked glycans in prion pathogenesis.Cell and tissue research · 2023Review
- Anchorless risk or released benefit? An updated view on the ADAM10-mediated shedding of the prion protein.Cell and tissue research · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Posttranslational modifications are a common feature of proteins associated with neurodegenerative diseases including prion protein (PrPC), tau, and α-synuclein. Alternative self-propagating protein states or strains give rise to different disease phenotypes and display strain-specific subsets of posttranslational modifications. The relationships between strain-specific structure, posttranslational modifications, and disease phenotype are poorly understood. We previously reported that among hundreds of PrPC sialoglycoforms expressed by a cell, individual prion strains recruited PrPC molecules selectively, according to the sialylation status of their N-linked glycans. Here we report that transmission of a prion strain to a new host is accompanied by a dramatic shift in the selectivity of recruitment of PrPC sialoglycoforms, giving rise to a self-propagating scrapie isoform (PrPSc) with a unique sialoglycoform signature and disease phenotype. The newly emerged strain has the shortest incubation time to disease and is characterized by colocalization of PrPSc with microglia and a very profound proinflammatory response, features that are linked to a unique sialoglycoform composition of PrPSc. The current work provides experimental support for the hypothesis that strain-specific patterns of PrPSc sialoglycoforms formed as a result of selective recruitment dictate strain-specific disease phenotypes. This work suggests a causative relationship between a strain-specific structure, posttranslational modifications, and disease phenotype.
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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.