Evidence map›Paper›PMID 36254605›Full record

ArticleThe EMBO journal2022

An arrayed genome-wide perturbation screen identifies the ribonucleoprotein Hnrnpk as rate-limiting for prion propagation.

Merve Avar, Daniel Heinzer, Alana M Thackray, Yingjun Liu, Marian Hruska-Plochan, Stefano Sellitto, Elke Schaper, Daniel P Pease, Jiang-An Yin, Asvin Kk Lakkaraju and 7 more

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

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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

17 authors at 2 institutions in 2 countries.

Merve Avar *Institute of Neuropathology, University of Zurich, Zurich, Switzerland.ORCID 0000-0003-4665-5558
Daniel Heinzer *Institute of Neuropathology, University of Zurich, Zurich, Switzerland.ORCID 0000-0002-3282-4042
Alana M ThackrayDepartment of Veterinary Medicine, University of Cambridge, Cambridge, UK.ORCID 0000-0002-2752-1127
Yingjun LiuInstitute of Neuropathology, University of Zurich, Zurich, Switzerland.ORCID 0000-0003-1543-1965
Marian Hruska-PlochanDepartment of Quantitative Biomedicine, University of Zurich, Zurich, Switzerland.ORCID 0000-0002-9253-4362
Stefano SellittoInstitute of Neuropathology, University of Zurich, Zurich, Switzerland.ORCID 0000-0003-2579-6271
Elke SchaperInstitute of Neuropathology, University of Zurich, Zurich, Switzerland.ORCID 0000-0003-3734-2496
Daniel P PeaseInstitute of Neuropathology, University of Zurich, Zurich, Switzerland.ORCID 0000-0001-6632-7063
Jiang-An YinInstitute of Neuropathology, University of Zurich, Zurich, Switzerland.ORCID 0000-0002-2134-8693
Asvin Kk LakkarajuInstitute of Neuropathology, University of Zurich, Zurich, Switzerland.ORCID 0000-0001-8752-148X
Marc EmmeneggerInstitute of Neuropathology, University of Zurich, Zurich, Switzerland.ORCID 0000-0002-6073-8811
Marco LosaInstitute of Neuropathology, University of Zurich, Zurich, Switzerland.ORCID 0000-0003-3428-418X
Andra ChincisanInstitute of Neuropathology, University of Zurich, Zurich, Switzerland.
Simone HornemannInstitute of Neuropathology, University of Zurich, Zurich, Switzerland.ORCID 0000-0002-2674-9891
Magdalini PolymenidouDepartment of Quantitative Biomedicine, University of Zurich, Zurich, Switzerland.ORCID 0000-0003-1271-9445
Raymond BujdosoDepartment of Veterinary Medicine, University of Cambridge, Cambridge, UK.
Adriano AguzziInstitute of Neuropathology, University of Zurich, Zurich, Switzerland.ORCID 0000-0002-0344-6708
University of Zurich · CHUniversity of Cambridge · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A defining characteristic of mammalian prions is their capacity for self-sustained propagation. Theoretical considerations and experimental evidence suggest that prion propagation is modulated by cell-autonomous and non-autonomous modifiers. Using a novel quantitative phospholipase protection assay (QUIPPER) for high-throughput prion measurements, we performed an arrayed genome-wide RNA interference (RNAi) screen aimed at detecting cellular host-factors that can modify prion propagation. We exposed prion-infected cells in high-density microplates to 35,364 ternary pools of 52,746 siRNAs targeting 17,582 genes representing the majority of the mouse protein-coding transcriptome. We identified 1,191 modulators of prion propagation. While 1,151 modified the expression of both the pathological prion protein, PrP

Indexed as

Prion DiseasesPrionsAnimalsDrosophila melanogasterMammalsMiceRibonucleoproteinsRNA InterferenceRNA, Small InterferingSheepPrionsRibonucleoproteinsRNA, Small InterferingHigh-throughput screenHnrnpkNeurodegenerationPrionProtein aggregation

Identifiers

PMID36254605
PMCPMC9713719
OpenAlexW4306679353

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.