ArticleFrontiers in cellular and infection microbiology2017
HA Triggers the Switch from MEK1 SUMOylation to Phosphorylation of the ERK Pathway in Influenza A Virus-Infected Cells and Facilitates Its Infection.
Article in Frontiers in cellular and infection microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Proteomics Analysis of Duck Lung Tissues in Response to Highly Pathogenic Avian Influenza Virus.Microorganisms · 2024Article
- The Immunosuppressive Roles of PD-L1 during Influenza A Virus Infection.International journal of molecular sciences · 2023Article
- MEK inhibitors as novel host-targeted antivirals with a dual-benefit mode of action against hyperinflammatory respiratory viral diseases.Current opinion in virology · 2023Review
- Exploring the role of Xingren on COVID-19 based on network pharmacology and molecular docking.Journal of food biochemistry · 2022Article
- NCommunications biology · 2022Article
- The Two Sides of the Same Coin-Influenza Virus and Intracellular Signal Transduction.Cold Spring Harbor perspectives in medicine · 2021Review
- Alternative Experimental Models for Studying Influenza Proteins, Host-Virus Interactions and Anti-Influenza Drugs.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Immune responses in influenza A virus and human coronavirus infections: an ongoing battle between the virus and host.Current opinion in virology · 2018Review
- Geldanamycin Reduces Acute Respiratory Distress Syndrome and Promotes the Survival of Mice Infected with the Highly Virulent H5N1 Influenza Virus.Frontiers in cellular and infection microbiology · 2017Article
- Vemurafenib Limits Influenza A Virus Propagation by Targeting Multiple Signaling Pathways.Frontiers in microbiology · 2017Article
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several post-translational modifications in host cells are hijacked by pathogens to facilitate their propagation. A number of components of the influenza virus have been reported to be modified by small ubiquitin-like modifier (SUMO) proteins during infection. We hypothesized that the MAPK/ERK pathway could be modified by SUMO1 because the SUMOylation of MEK1 was quickly eliminated after influenza A virus infection. We identified host cell MEK1 as a target of SUMO1 through LC/MS/MS, and enhanced MEK1 SUMOylation inhibited the infection of the virus, while inhibition of host cell MEK1 SUMOylation facilitated virus propagation. Further investigation demonstrated that the MAPK/ERK pathway is downregulated by MEK1 SUMOylation, which is inhibited by influenza virus infection. Furthermore, membrane accumulation of hemagglutinin promoted MEK1 phosphorylation and gradually abrogated the MEK1 SUMOylation. Taken together, we report a possible mechanism in which HA may trigger the ERK pathway in influenza A virus-infected cells as the switch from MEK1 SUMOylation to phosphorylation, facilitating virus infection.
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