An arrayed genome-wide perturbation screen identifies the ribonucleoprotein Hnrnpk as rate-limiting for prion propagation.
High-throughput screen
Hnrnpk
Neurodegeneration
Prion
Protein aggregation
Journal
The EMBO journal
ISSN: 1460-2075
Titre abrégé: EMBO J
Pays: England
ID NLM: 8208664
Informations de publication
Date de publication:
01 12 2022
01 12 2022
Historique:
revised:
17
09
2022
received:
10
08
2022
accepted:
22
09
2022
pubmed:
19
10
2022
medline:
3
12
2022
entrez:
18
10
2022
Statut:
ppublish
Résumé
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
Identifiants
pubmed: 36254605
doi: 10.15252/embj.2022112338
pmc: PMC9713719
doi:
Substances chimiques
Prions
0
Ribonucleoproteins
0
RNA, Small Interfering
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e112338Informations de copyright
©2022 The Authors. Published under the terms of the CC BY NC ND 4.0 license.
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