ArticleJournal of virology2004
PB1-F2, an influenza A virus-encoded proapoptotic mitochondrial protein, creates variably sized pores in planar lipid membranes.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 146 citations in OpenAlex.
- Computational Insights into PB1-F2 Mediated Modulation of VDAC1: An Allosteric Mechanism in Mitochondrial Dysfunction.ACS omega · 2026Article
- Innate immune role of IL-6 in influenza a virus pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- Genomic characterization of equine influenza A subtype H3N8 viruses by long read sequencing and functional analyses of the PB1-F2 virulence factor of A/equine/Paris/1/2018.Veterinary research · 2024Article
- Severe acute respiratory syndrome coronaviruses contributing to mitochondrial dysfunction: Implications for post-COVID complications.Mitochondrion · 2023Review
- Voltage-dependent anion channel 2 (VDAC2) facilitates the accumulation of rice stripe virus in the vector Laodelphax striatellus.Virus research · 2023Article
- PB1F2 from Influenza A Virus Regulates the Interaction between Cytochrome C and Cardiolipin.Membranes · 2022Article
- A Game of Infection - Song of Respiratory Viruses and Interferons.Frontiers in cellular and infection microbiology · 2022Review
- Calcium Ions Signaling: Targets for Attack and Utilization by Viruses.Frontiers in microbiology · 2022Review
- Endoplasmic reticulum & mitochondrial calcium homeostasis: The interplay with viruses.Mitochondrion · 2021Article
- Roles of the Non-Structural Proteins of Influenza A Virus.Pathogens (Basel, Switzerland) · 2020Review
- Impact of COVID-19 on Mitochondrial-Based Immunity in Aging and Age-Related Diseases.Frontiers in aging neuroscience · 2020Review
- Artificial Cell Membranes Interfaced with Optical Tweezers: A Versatile Microfluidics Platform for Nanomanipulation and Mechanical Characterization.ACS applied materials & interfaces · 2019Article
- Virulent PB1-F2 residues: effects on fitness of H1N1 influenza A virus in mice and changes during evolution of human influenza A viruses.Scientific reports · 2018Article
- Influenza Virus: A Master Tactician in Innate Immune Evasion and Novel Therapeutic Interventions.Frontiers in immunology · 2018Review
- Evolution and Virulence of Influenza A Virus Protein PB1-F2.International journal of molecular sciences · 2017Review
- Effects of PB1-F2 on the pathogenicity of H1N1 swine influenza virus in mice and pigs.The Journal of general virology · 2017Article
- Computational models for monitoring the trans-membrane potential with fluorescent probes: the DiSCEuropean biophysics journal : EBJ · 2016Article
- The PB2 Subunit of the Influenza A Virus RNA Polymerase Is Imported into the Mitochondrial Matrix.Journal of virology · 2016Article
- Pro-apoptotic Bax molecules densely populate the edges of membrane pores.Scientific reports · 2016Article
- Amyloid Assemblies of Influenza A Virus PB1-F2 Protein Damage Membrane and Induce Cytotoxicity.The Journal of biological chemistry · 2016Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 6 institutions in 5 countries.
Funding
Abstract
A frameshifted region of the influenza A virus PB1 gene encodes a novel protein, termed PB1-F2, a mitochondrial protein that can induce cell death. Many proapoptotic proteins are believed to act at the mitochondrial outer membrane to form an apoptotic pore with lipids. We studied the interaction of isolated, synthetic PB1-F2 (sPB1-F2) peptide with planar phospholipid bilayer membranes. The presence of nanomolar concentrations of peptide in the bathing solution induced a transmembrane conductance that increased in a potential-dependent manner. Positive potential on the side of protein addition resulted in a severalfold increase in the rate of change of membrane conductance. sPB1-F2-treated membranes became permeable to monovalent cations, chloride, and to a lesser extent, divalent ions. Despite various experimental conditions, we did not detect the distinctive conductance levels typical of large, stable pores, protein channels, or even pores that are partially proteinaceous. Rather, membrane conductance induced by sPB1-F2 fluctuated and visited almost all conductance values. sPB1-F2 also dramatically decreased bilayer stability in an electric field, consistent with a decrease in the line tension of a lipidic pore. Since similar membrane-destabilizing profiles are seen with proapoptotic proteins (e.g., Bax) and the cytoplasmic helix of human immunodeficiency virus gp41, we suggest that the basis for sPB1-F2-induced cell death may be the permeabilization and destabilization of mitochondrial membranes, leading to macromolecular leakage and apoptosis.
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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.