Evidence map›Paper›PMID 39677672›Full record

ArticlebioRxiv : the preprint server for biology2024

Ubiquitin Ligase ITCH Regulates Life Cycle of SARS-CoV-2 Virus.

Qiwang Xiang, Camille Wouters, Peixi Chang, Yu-Ning Lu, Mingming Liu, Haocheng Wang, Junqin Yang, Andrew Pekosz, Yanjin Zhang, Jiou Wang

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Qiwang XiangDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, 21205, USA.
Camille WoutersDepartment of Molecular Microbiology & Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, 21205, USA.
Peixi ChangDepartment of Veterinary Medicine, University of Maryland, College Park, MD, 20742, USA.
Yu-Ning LuDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, 21205, USA.
Mingming LiuDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, 21205, USA.
Haocheng WangDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, 21205, USA.
Junqin YangDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, 21205, USA.
Andrew PekoszDepartment of Molecular Microbiology & Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, 21205, USA.ORCID 0000-0003-3248-1761
Yanjin ZhangDepartment of Veterinary Medicine, University of Maryland, College Park, MD, 20742, USA.
Jiou WangDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, 21205, USA.ORCID 0000-0001-9115-8708

Funding

Neurodegeneration and Proteotoxicity Dissected in C. elegans and MammalsR01NS074324 · NINDS · JOHNS HOPKINS UNIVERSITY · PI WANG, JIOU · 2011 to 2025
$6.2M
NINDS NIH HHS R01 NS074324
6 · The paper itself

Abstract

SARS-CoV-2 infection poses a major threat to public health, and understanding the mechanism of viral replication and virion release would help identify therapeutic targets and effective drugs for combating the virus. Herein, we identified E3 ubiquitin-protein ligase Itchy homolog (ITCH) as a central regulator of SARS-CoV-2 at multiple steps and processes. ITCH enhances the ubiquitination of viral envelope and membrane proteins and mutual interactions of structural proteins, thereby aiding in virion assembly. ITCH-mediated ubiquitination also enhances the interaction of viral proteins to the autophagosome receptor p62, promoting their autophagosome-dependent secretion. Additionally, ITCH disrupts the trafficking of the protease furin and the maturation of cathepsin L, thereby suppressing their activities in cleaving and destabilizing the viral spike protein. Furthermore, ITCH exhibits robust activation during the SARS-CoV-2 replication stage, and SARS-CoV-2 replication is significantly decreased by genetic or pharmacological inhibition of ITCH. These findings provide new insights into the mechanisms of the SARS-CoV-2 life cycle and identify a potential target for developing treatments for the virus-related diseases.

Indexed as

envelope protein (E)Itchy E3 Ubiquitin Protein Ligase (ITCH)membrane protein (M)SARS-CoV-2spike protein (S)Ubiquitin

Identifiers

PMID39677672
PMCPMC11642887

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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.