ArticleCell death & disease2011
Cell death regulation during influenza A virus infection by matrix (M1) protein: a model of viral control over the cellular survival pathway.
Article in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
- Orchestrating immunopathology: the spectrum of programmed cell death pathways co-opted by influenza a virus in pulmonary immunity.Frontiers in immunology · 2026Review
- Comparative IP-MS Reveals HSPA5 and HSPA8 Interacting with Hemagglutinin Protein to Promote the Replication of Influenza A Virus.Pathogens (Basel, Switzerland) · 2025Article
- A genetically engineered therapeutic lectin inhibits human influenza A virus infection and sustains robust virus-specific CD8 T cell expansion.PLoS pathogens · 2025Article
- Triggering Degradation of Host Cellular Proteins for Robust Propagation of Influenza Viruses.International journal of molecular sciences · 2024Review
- Nontoxic Levels of Se-Containing Compounds Increase Survival by Blocking Oxidative and Inflammatory Stresses via Signal Pathways Whereas High Levels of Se Induce Apoptosis.Molecules (Basel, Switzerland) · 2023Review
- Influenza viral matrix 1 protein aggravates viral pathogenicity by inducing TLR4-mediated reactive oxygen species production and apoptotic cell death.Cell death & disease · 2023Article
- Diverse roles of lung macrophages in the immune response to influenza A virus.Frontiers in microbiology · 2023Review
- FBXO6 regulates the antiviral immune responses via mediating alveolar macrophages survival.Journal of medical virology · 2023Article
- The Contribution of Viral Proteins to the Synergy of Influenza and Bacterial Co-Infection.Viruses · 2022Review
- Innate immune sensing of influenza A viral RNA through IFI16 promotes pyroptotic cell death.iScience · 2022Article
- Visualizing Influenza A Virus vRNA Replication.Frontiers in microbiology · 2022Article
- Intracellular Redox-Modulated Pathways as Targets for Effective Approaches in the Treatment of Viral Infection.International journal of molecular sciences · 2021Review
- Potential Role of Antioxidant and Anti-Inflammatory Therapies to Prevent Severe SARS-Cov-2 Complications.Antioxidants (Basel, Switzerland) · 2021Review
- Molecular Events Involved in Influenza A Virus-Induced Cell Death.Frontiers in microbiology · 2021Review
- Can Activation of NRF2 Be a Strategy against COVID-19?Trends in pharmacological sciences · 2020Review
- Review
- Review
- Influenza A Virus Nucleoprotein Activates the JNK Stress-Signaling Pathway for Viral Replication by Sequestering Host Filamin A Protein.Frontiers in microbiology · 2020Article
- Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During early infection, viruses activate cellular stress-response proteins such as heat-shock proteins (Hsps) to counteract apoptosis, but later on, they modulate these proteins to stimulate apoptosis for efficient viral dissemination. Hsp70 has been attributed to modulate viral entry, transcription, nuclear translocation and virion formation. It also exerts its anti-apoptotic function by binding to apoptosis protease-activating factor 1 (Apaf-1) and disrupting apoptosome formation. Here, we show that influenza A virus can regulate the anti-apoptotic function of Hsp70 through viral protein M1 (matrix 1). M1 itself did not induce apoptosis, but enhanced the effects of apoptotic inducers. M1-small-interfering RNA inhibits virus-induced apoptosis in cells after either virus infection or overexpression of the M1 protein. M1 binds to Hsp70, which results in reduced interaction between Hsp70 and Apaf-1. In a cell-free system, the M1 protein mediates procaspase-9 activation induced by cytochrome c/deoxyadenosine triphosphate. A study involving deletion mutants confirmed the role of the C-terminus substrate-binding domain (EEVD) of Hsp70 and amino acids 128-165 of M1 for this association. The M1 mutants, which did not co-immunoprecipitate with Hsp70, failed to induce apoptosis. Overall, the study confirms the proapoptotic function of the M1 protein during influenza virus infection.
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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.