ArticleThe Journal of biological chemistry2009
Bcl-2 expression and p38MAPK activity in cells infected with influenza A virus: impact on virally induced apoptosis and viral replication.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 94 citations in OpenAlex.
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- Apoptosis as an evolutionary battleground: pathogen pressure and the shaping of programmed cell death pathways.Frontiers in cell and developmental biology · 2026Review
- Co-infection models ofFrontiers in cellular and infection microbiology · 2026Article
- Uukuniemi virus infection causes a pervasive remodelling of the RNA-binding proteome in tick cells.PLoS pathogens · 2025Article
- BIK polymorphism and proteasome regulation unveil host risk factor for severe influenza.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Originally Established PBE Cell Line as a Reliable In Vitro Model for Investigating SIV Infection and Immunity.International journal of molecular sciences · 2025Article
- Uncovering the Mechanisms of BaBaoWuDanYaoMo Against Influenza A Virus and Virus-Induced Inflammation Based on Network Pharmacology and Pharmacological Evaluation.Infection and drug resistance · 2025Article
- Review of the potential pharmacological role of erucic acid: a monounsaturated omega-9 fatty acid.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Prognostic and immune correlation analysis of mitochondrial autophagy and aging-related genes in lung adenocarcinoma.Journal of cancer research and clinical oncology · 2023Article
- Dysregulation of intracellular redox homeostasis by the SARS-CoV-2 ORF6 protein.Virology journal · 2023Article
- Independent role of caspases and Bik in augmenting influenza A virus replication in airway epithelial cells and mice.Virology journal · 2023Article
- A Comprehensive Survey on the Expediated Anti-COVID-19 Options Enabled by Metal Complexes-Tasks and Trials.Molecules (Basel, Switzerland) · 2023Review
- Involvement of AMPKα and MAPK-ERK/-JNK Signals in Docetaxel-Induced Human Tongue Squamous Cell Carcinoma Cell Apoptosis.International journal of molecular sciences · 2022Article
- 5-Methoxyflavone-induced AMPKα activation inhibits NF-κB and P38 MAPK signaling to attenuate influenza A virus-mediated inflammation and lung injury in vitro and in vivo.Cellular & molecular biology letters · 2022Article
- Integrated analysis to study the interplay between post-translational modifications (PTM) in hepatitis C virus proteins and hepatocellular carcinoma (HCC) development.Scientific reports · 2022Article
- Nitrostilbenes: Synthesis and Biological Evaluation as Potential Anti-Influenza Virus Agents.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Metal-based complexes against SARS-CoV-2.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2022Review
- Development of Metal Complexes for Treatment of Coronaviruses.International journal of molecular sciences · 2022Article
- Quercetin induces tongue squamous cell carcinoma cell apoptosis via the JNK activation-regulated ERK/GSK-3α/β-mediated mitochondria-dependent apoptotic signaling pathway.Oncology letters · 2022Article
- MK2a inhibitor CMPD1 abrogates chikungunya virus infection by modulating actin remodeling pathway.PLoS pathogens · 2021Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous reports have shown that various steps in the influenza A virus life cycle are impaired in cells expressing the antiapoptotic protein Bcl-2 (Bcl-2(+) cells). We demonstrated a direct link between Bcl-2 and the reduced nuclear export of viral ribonucleoprotein (vRNP) complexes in these cells. However, despite its negative impact on viral replication, Bcl-2 did not prevent host cells from undergoing virally triggered apoptosis. The protein's reduced antiapoptotic capacity was related to phosphorylation of its threonine 56 and serine 87 residues by virally activated p38MAPK. In infected Bcl-2(+) cells, activated p38MAPK was found predominantly in the cytoplasm, colocalized with Bcl-2, and both Bcl-2 phosphorylation and virally induced apoptosis were diminished by specific inhibition of p38MAPK activity. In contrast, in Bcl-2-negative (Bcl-2(-)) cells, which are fully permissive to viral infection, p38MAPK activity was predominantly nuclear, and its inhibition decreased vRNP traffic, phosphorylation of viral nucleoprotein, and virus titers in cell supernatants, suggesting that this kinase also contributes to the regulation of vRNP export and viral replication. This could explain why in Bcl-2(+) cells, where p38MAPK is active in the cytoplasm, phosphorylating Bcl-2, influenza viral replication is substantially reduced, whereas apoptosis proceeds at rates similar to those observed in Bcl-2(-) cells. Our findings suggest that the impact of p38MAPK on the influenza virus life cycle and the apoptotic response of host cells to infection depends on whether or not the cells express Bcl-2, highlighting the possibility that the pathological effects of the virus are partly determined by the cell type it targets.
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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.