Evidence map›Paper›PMID 36511154›Full record

ArticleJournal of neurochemistry2023

A single protective polymorphism in the prion protein blocks cross-species prion replication in cultured cells.

Hamza Arshad, Zeel Patel, Genki Amano, Le Yao Li, Zaid A M Al-Azzawi, Surachai Supattapone, Gerold Schmitt-Ulms, Joel C Watts

Open access · greenAbstract read
In one paragraph

Article in Journal of neurochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 22% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A Neuronal Cell Line Model for Studying Camel Prions.Pathogens (Basel, Switzerland) · 2026
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Hamza ArshadTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada.
Zeel PatelTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada.
Genki AmanoTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada.
Le Yao LiTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada.
Zaid A M Al-AzzawiTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada.
Surachai SupattaponeDepartment of Biochemistry, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, USA.
Gerold Schmitt-UlmsTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada.
Joel C WattsTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada.ORCID 0000-0002-2604-2925
University of Toronto · CADartmouth College · US

Funding

Mapping Molecular Pathways that Control Prion MetabolismR37NS125431 · NINDS · DARTMOUTH COLLEGE · PI Surachai Supattapone · 2022 to 2026
$3.5M
Structural Mechanism of Mammalian Prion InfectivityR01NS118796 · NINDS · DARTMOUTH COLLEGE · PI SUPATTAPONE, SURACHAI, ZILM, KURT WILLIAM · 2020 to 2024
$2.8M
Novel Therapeutic Strategies Targeting Malleability of Wild-Type and Mutant PrionsR01NS117276 · NINDS · DARTMOUTH COLLEGE · PI SUPATTAPONE, SURACHAI · 2020 to 2025
$2.4M
Dissecting the Mechanism of Prion Formation with a Permissive HostR01NS102301 · NINDS · DARTMOUTH COLLEGE · PI SUPATTAPONE, SURACHAI · 2018 to 2021
$2.2M
NINDS NIH HHS R01 NS102301NINDS NIH HHS R01 NS117276NINDS NIH HHS R01 NS118796NINDS NIH HHS R37 NS125431
6 · The paper itself

Abstract

The bank vole (BV) prion protein (PrP) can function as a universal acceptor of prions. However, the molecular details of BVPrP's promiscuity for replicating a diverse range of prion strains remain obscure. To develop a cultured cell paradigm capable of interrogating the unique properties of BVPrP, we generated monoclonal lines of CAD5 cells lacking endogenous PrP but stably expressing either hamster (Ha), mouse (Mo), or BVPrP (M109 or I109 polymorphic variants) and then challenged them with various strains of mouse or hamster prions. Cells expressing BVPrP were susceptible to both mouse and hamster prions, whereas cells expressing MoPrP or HaPrP could only be infected with species-matched prions. Propagation of mouse and hamster prions in cells expressing BVPrP resulted in strain adaptation in several instances, as evidenced by alterations in conformational stability, glycosylation, susceptibility to anti-prion small molecules, and the inability of BVPrP-adapted mouse prion strains to infect cells expressing MoPrP. Interestingly, cells expressing BVPrP containing the G127V prion gene variant, identified in individuals resistant to kuru, were unable to become infected with prions. Moreover, the G127V polymorphic variant impeded the spontaneous aggregation of recombinant BVPrP. These results demonstrate that BVPrP can facilitate cross-species prion replication in cultured cells and that a single amino acid change can override the prion-permissive nature of BVPrP. This cellular paradigm will be useful for dissecting the molecular features of BVPrP that allow it to function as a universal prion acceptor.

Indexed as

Prion DiseasesPrionsAnimalsArvicolinaeCells, CulturedCricetinaePrion ProteinsPrion ProteinsPrionscultured cellsneurodegenerative diseasesprionprotein misfolding

Identifiers

PMID36511154
PMCPMC11806934
OpenAlexW4311237385

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.