ArticleJournal of virology2019
The NS1 Protein of Influenza A Virus Participates in Necroptosis by Interacting with MLKL and Increasing Its Oligomerization and Membrane Translocation.
Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- Targeting MLKL-Driven Necroptosis: A Therapeutic Target in Inflammation and Host Defense.Biomolecules · 2026Review
- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
- Pre-activation timing determines influenza severity and viral pathogenicity via STING Inhibition.Scientific reports · 2025Article
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- Mixed Lineage Kinase Domain-Like Protein (MLKL): From Mechanisms to Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Pristimerin ameliorates colitis‑induced intestinal mucosal injury by inhibiting intestinal epithelial necroptosis.Molecular medicine reports · 2025Article
- The role of programmed cell death in organ dysfunction induced by opportunistic pathogens.Critical care (London, England) · 2025Review
- Mechanistic Insights into Influenza A Virus-Induced Cell Death and Emerging Treatment Strategies.Veterinary sciences · 2024Review
- Influenza virus infection activates TAK1 to suppress RIPK3-independent apoptosis and RIPK1-dependent necroptosis.Cell communication and signaling : CCS · 2024Article
- Review
- RIPK3 promotes hantaviral replication by restricting JAK-STAT signaling without triggering necroptosis.Virologica Sinica · 2023Article
- Interaction among inflammasome, PANoptosise, and innate immune cells in infection of influenza virus: Updated review.Immunity, inflammation and disease · 2023Review
- Role of CIV NS1 Protein in Innate Immunity and Viral Replication.International journal of molecular sciences · 2023Article
- The double-edged functions of necroptosis.Cell death & disease · 2023Review
- MLKL post-translational modifications: road signs to infection, inflammation and unknown destinations.Cell death and differentiation · 2023Review
- Race between virus and inflammasomes: inhibition or escape, intervention and therapy.Frontiers in cellular and infection microbiology · 2023Review
- Regulated necrosis, a proinflammatory cell death, potentially counteracts pathogenic infections.Cell death & disease · 2022Review
- Innate immune sensing of influenza A viral RNA through IFI16 promotes pyroptotic cell death.iScience · 2022Article
- Influenza A Virus Infection Activates NLRP3 Inflammasome through Trans-Golgi Network Dispersion.Viruses · 2022Article
- TNF-mediated alveolar macrophage necroptosis drives disease pathogenesis during respiratory syncytial virus infection.The European respiratory journal · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elimination of infected cells by programmed cell death is a well-recognized host defense mechanism to control the spread of infection. In addition to apoptosis, necroptosis is also one of the mechanisms of cell death that can be activated by viral infection. Activation of necroptosis leads to the phosphorylation of mixed-lineage kinase domain-like protein (MLKL) by receptor-interacting protein kinase 3 (RIPK3) and results in MLKL oligomerization and membrane translocation, leading to membrane disruption and a loss of cellular ion homeostasis. It has recently been reported that influenza A virus (IAV) infection induces necroptosis. However, the underlying mechanism of the IAV-mediated necroptosis process, particularly the roles of IAV proteins in necroptosis, remains unexplored. Here, we report that IAV infection induces necroptosis in macrophages and epithelial cells. We demonstrate that the NS1 protein of IAV interacts with MLKL. Coiled-coil domain 2 of MLKL has a predominant role in mediating the MLKL interaction with NS1. The interaction of NS1 with MLKL increases MLKL oligomerization and membrane translocation. Moreover, the MLKL-NS1 interaction enhances MLKL-mediated NLRP3 inflammasome activation, leading to increased interleukin-1β (IL-1β) processing and secretion.
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Registered trials
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.