Evidence map›Paper›PMID 37683630›Full record

ArticleDevelopmental cell2023

Usp25-Erlin1/2 activity limits cholesterol flux to restrict virus infection.

Qi Wen Teo, Ho Him Wong, Tiaan Heunis, Viktoriya Stancheva, Asmaa Hachim, Huibin Lv, Lewis Siu, Julian Ho, Yun Lan, Chris Ka Pun Mok and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Developmental cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
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  4. TRIM21 is a molecular rheostat for influenza A virus replication.bioRxiv : the preprint server for biology · 2026
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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

12 authors at 4 institutions in 3 countries.

Qi Wen TeoHKU-Pasteur Research Pole, School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China; Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
Ho Him WongHKU-Pasteur Research Pole, School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Tiaan HeunisSir William Dunn School of Pathology, South Parks Road, University of Oxford, Oxford OX1 3RE, UK.
Viktoriya StanchevaSir William Dunn School of Pathology, South Parks Road, University of Oxford, Oxford OX1 3RE, UK.
Asmaa HachimSir William Dunn School of Pathology, South Parks Road, University of Oxford, Oxford OX1 3RE, UK.
Huibin LvHKU-Pasteur Research Pole, School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Lewis SiuHKU-Pasteur Research Pole, School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Julian HoHKU-Pasteur Research Pole, School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Yun LanHKU-Pasteur Research Pole, School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Chris Ka Pun MokHKU-Pasteur Research Pole, School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Rachel UlfertsThe Francis Crick Institute, London, UK.
Sumana SanyalSir William Dunn School of Pathology, South Parks Road, University of Oxford, Oxford OX1 3RE, UK; HKU-Pasteur Research Pole, School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. Electronic address: sumana.sanyal@path.ox.ac.uk.
HKU-Pasteur Research Pole · HKUniversity of Oxford · GBThe Francis Crick Institute · GBUniversity of Illinois Urbana-Champaign · US

Funding

Wellcome TrustWellcome Trust 220776/Z/20/ZWellcome Trust 223107/Z/21/Z
6 · The paper itself

Abstract

Reprogramming lipid metabolic pathways is a critical feature of activating immune responses to infection. However, how these reconfigurations occur is poorly understood. Our previous screen to identify cellular deubiquitylases (DUBs) activated during influenza virus infection revealed Usp25 as a prominent hit. Here, we show that Usp25-deleted human lung epithelial A549 cells display a >10-fold increase in pathogenic influenza virus production, which was rescued upon reconstitution with the wild type but not the catalytically deficient (C178S) variant. Proteomic analysis of Usp25 interactors revealed a strong association with Erlin1/2, which we confirmed as its substrate. Newly synthesized Erlin1/2 were degraded in Usp25

Indexed as

CholesterolUbiquitin ThiolesteraseVirus DiseasesHumansLipidsLungMembrane ProteinsNerve Tissue ProteinsProteomicsCholesterolERLIN1 protein, humanERLIN2 protein, humanLipidsMembrane ProteinsNerve Tissue ProteinsUbiquitin ThiolesteraseUSP25 protein, humanautophagycholesterolErlin1/2influenzainnate immunitylipid homeostasisUsp25

Identifiers

PMID37683630
PMCPMC10914638
OpenAlexW4386496667

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.