ArticleAmerican journal of physiology. Lung cellular and molecular physiology2023
Influenza virus reduces ubiquitin E3 ligase MARCH10 expression to decrease ciliary beat frequency.
Article in American journal of physiology. Lung cellular and molecular physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Review
- Post-translational modification networks as master regulators of influenza virus replication, host adaptation, and immune evasion.Frontiers in immunology · 2026Review
- MARCH E3 Ligases: Understudied Regulators of Pulmonary Immune Function.Journal of respiratory biology and translational medicine · 2026Article
- Ubiquitin E3 ligase MARCH10 targets influenza hemagglutinin for ubiquitination.Cellular signalling · 2025Article
- Lung cell fates during influenza.Cell research · 2025Review
- SomaticiScience · 2025Article
- Interplay between respiratory viruses and cilia in the airways.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Unraveling Novel Strategies: Targeting Miz1 for Degradation to Enhance Antiviral Defense against Influenza A Virus.Journal of respiratory biology and translational medicine · 2024Article
- Concurrent loss of ciliary genesRoyal Society open science · 2023Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Respiratory viruses, such as influenza, decrease airway cilia function and expression, which leads to reduced mucociliary clearance and inhibited overall immune defense. Ubiquitination is a posttranslational modification using E3 ligases, which plays a role in the assembly and disassembly of cilia. We examined the role of membrane-associated RING-CH (MARCH) family of E3 ligases during influenza infection and determined that MARCH10, specifically expressed in ciliated epithelial cells, is significantly decreased during influenza infection in mice, human lung epithelial cells, and human lung tissue. Cellular depletion of MARCH10 in differentiated human bronchial epithelial cells (HBECs) using CRISPR/Cas9 showed a decrease in ciliary beat frequency. Furthermore, MARCH10 cellular knockdown in combination with influenza infection selectively decreased immunoreactive levels of the ciliary component, dynein axonemal intermediate chain 1. Cellular overexpression of MARCH10 significantly decreased influenza hemagglutinin protein levels in the differentiated HBECs and knockdown of MARCH10 increased IL-1β cytokine expression, whereas overexpression had the reciprocal effect. These findings suggest that MARCH10 may have a protective role in airway pulmonary host defense and innate immunity during influenza infection.
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Registered trials
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