Evidence map›Paper›PMID 39505910›Full record

ArticleNature communications2024

AMFR-mediated Flavivirus NS2A ubiquitination subverts ER-phagy to augment viral pathogenicity.

Linliang Zhang, Hongyun Wang, Chao Han, Qi Dong, Jie Yan, Weiwei Guo, Chao Shan, Wen Zhao, Pu Chen, Rui Huang and 4 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

  1. Review
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  18. Article
  19. Organoids: physiologically relevantJournal of virology · 2025
    Review
  20. Article
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

14 authors.

Linliang Zhang *School of Life Sciences, Hubei University, Wuhan, 430062, China.ORCID 0009-0001-6021-9050
Hongyun Wang *State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Chao HanState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Qi DongState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Jie YanState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Weiwei GuoState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430072, China.
Chao ShanState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430072, China.ORCID 0000-0002-3953-3782
Wen ZhaoTissue Engineering and Organ Manufacturing (TEOM) Lab, Department of Biomedical Engineering, Wuhan University Taikang Medical School (School of Basic Medical Sciences), Wuhan, 430072, China.
Pu ChenTissue Engineering and Organ Manufacturing (TEOM) Lab, Department of Biomedical Engineering, Wuhan University Taikang Medical School (School of Basic Medical Sciences), Wuhan, 430072, China.ORCID 0000-0002-6857-2211
Rui HuangState Key Laboratory of Virology and Hubei Province Key Laboratory of Allergy and Immunology, Institute of Medical Virology, TaiKang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan, 430072, China.ORCID 0000-0002-8299-1471
Ying WuState Key Laboratory of Virology and Hubei Province Key Laboratory of Allergy and Immunology, Institute of Medical Virology, TaiKang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan, 430072, China.
Yu ChenState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, China. chenyu@whu.edu.cn.ORCID 0000-0003-1300-4652
Yali QinSchool of Life Sciences, Hubei University, Wuhan, 430062, China. yqin@hubu.edu.cn.
Mingzhou ChenSchool of Life Sciences, Hubei University, Wuhan, 430062, China. chenmz@hubu.edu.cn.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32200127
6 · The paper itself

Abstract

Flaviviruses strategically utilize the endoplasmic reticulum (ER) in their replication cycles. However, the role of ER autophagy (ER-phagy) in viral replication process remains poorly understood. Here, we reveal that prolonged Zika virus (ZIKV) infection results from the degradation of ER-phagy receptor FAM134B, facilitated by viral NS2A protein. Mechanistically, ER-localized NS2A undergoes K48-linked polyubiquitination at lysine (K) 56 by E3 ligase AMFR. Ubiquitinated NS2A binds to FAM134B and AMFR orchestrates the degradation of NS2A-FAM134B complexes. AMFR-catalyzed NS2A ubiquitination not only targets FAM134B degradation but also hinders the FAM134B-AMFR axis. Notably, a recombinant ZIKV mutant (ZIKV-NS2A

Indexed as

AutophagyEndoplasmic ReticulumMembrane ProteinsReceptors, Autocrine Motility FactorViral Nonstructural ProteinsZika VirusZika Virus InfectionAnimalsCell LineChlorocebus aethiopsDisease Models, AnimalFemaleHumansIntracellular Signaling Peptides and ProteinsMaleMiceAMFR protein, humanAmfr protein, mouseFam134b protein, mouseIntracellular Signaling Peptides and ProteinsMembrane ProteinsPOLY protein, Zika virusReceptors, Autocrine Motility FactorRETREG1 protein, humanViral Nonstructural Proteins

Identifiers

PMID39505910
PMCPMC11541587

What OpenQuestion holds

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Registered trials

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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.