ArticleSignal transduction and targeted therapy2022
Multiomics approach reveals the ubiquitination-specific processes hijacked by SARS-CoV-2.
Article in Signal transduction and targeted therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Identifying and profiling structural similarities between Spike of SARS-CoV-2 and other viral or host proteins with Machaon.Communications biology · 2023Pooled it
- SARS-CoV-2 ORF3a suppresses host antiviral interferon responses by promoting STUB1-mediated PTEN proteasomal degradation.Journal of virology · 2026Article
- O-GlcNAcylation licenses RNF166 to degrade the M protein of porcine coronaviruses.PLoS pathogens · 2026Article
- Ubiquitination and autophagy in host-pathogen interactions: from immune surveillance to therapeutic targeting.Nature reviews. Immunology · 2026Review
- Rewriting the viral script: post-translational modifications orchestrating SARS-CoV-2 pathogenesis and immune evasion.Frontiers in microbiology · 2026Review
- Structural and Computational Insights into the Attenuated Innate Immune Recognition of the SARS-CoV-2 N15 Lineage, an Early-Pandemic Variant.Computational and structural biotechnology journal · 2026Article
- UBXN7 facilitates SARS-CoV-2 replication via inhibiting the K48-linked ubiquitination of viral N protein.PLoS pathogens · 2025Article
- scDETECT: a novel statistical model accounting for cell type correlation in single-cell RNA-seq differential expression analysis.Briefings in bioinformatics · 2025Article
- Linear Ubiquitination of Hemocyanin Mediated by LUBEL Regulates Innate Immunity inInternational journal of molecular sciences · 2025Article
- Article
- Mutational pressure promotes release of public CD8iScience · 2025Article
- Proteome-wide characterization of PTMs reveals host cell responses to viral infection and identifies putative antiviral drug targets.Frontiers in immunology · 2025Review
- SUMOylation of SARS-CoV-2 spike protein is a key target for broad-spectrum antiviral therapy.Theranostics · 2025Article
- Multi-proteomics and interactome dataset of tick-borne encephalitis virus infected host cells.Scientific data · 2024Article
- Lung-Targeted Lipid Nanoparticle-Delivered siUSP33 Attenuates SARS-CoV-2 Replication and Virulence by Promoting Envelope Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Human E3 ubiquitin ligases: accelerators and brakes for SARS-CoV-2 infection.Biochemical Society transactions · 2024Review
- Article
- Genome-scale CRISPR-Cas9 screen identifies host factors as potential therapeutic targets for SARS-CoV-2 infection.iScience · 2024Article
- A Cullin 5-based complex serves as an essential modulator of ORF9b stability in SARS-CoV-2 replication.Signal transduction and targeted therapy · 2024Article
- LLPS of FXR proteins drives replication organelle clustering for β-coronaviral proliferation.The Journal of cell biology · 2024Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Coronavirus Disease 2019 (COVID-19) caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is a global pandemic that seriously threatens health and socioeconomic development, but the existed antiviral drugs and vaccines still cannot yet halt the spread of the epidemic. Therefore, a comprehensive and profound understanding of the pathogenesis of SARS-CoV-2 is urgently needed to explore effective therapeutic targets. Here, we conducted a multiomics study of SARS-CoV-2-infected lung epithelial cells, including transcriptomic, proteomic, and ubiquitinomic. Multiomics analysis showed that SARS-CoV-2-infected lung epithelial cells activated strong innate immune response, including interferon and inflammatory responses. Ubiquitinomic further reveals the underlying mechanism of SARS-CoV-2 disrupting the host innate immune response. In addition, SARS-CoV-2 proteins were found to be ubiquitinated during infection despite the fact that SARS-CoV-2 itself didn't code any E3 ligase, and that ubiquitination at three sites on the Spike protein could significantly enhance viral infection. Further screening of the E3 ubiquitin ligases and deubiquitinating enzymes (DUBs) library revealed four E3 ligases influencing SARS-CoV-2 infection, thus providing several new antiviral targets. This multiomics combined with high-throughput screening study reveals that SARS-CoV-2 not only modulates innate immunity, but also promotes viral infection, by hijacking ubiquitination-specific processes, highlighting potential antiviral and anti-inflammation targets.
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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.