ArticleJournal of virology2008
Vaccinia virus A56/K2 fusion regulatory protein interacts with the A16 and G9 subunits of the entry fusion complex.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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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
44 citing papers in PubMed, 61 citations in OpenAlex.
- Immunogenicity of poxvirus A16/G9 entry-fusion subcomplex and its restriction by A56/K2 protein informs vaccine design.Nature microbiology · 2026Article
- Structural basis of mpox virus A30/H2 subcomplex formation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cryo-EM structure of the vaccinia virus entry fusion complex reveals a multicomponent fusion machinery.Science advances · 2026Article
- Review
- Lumpy Skin Disease Virus Pathogenesis: Viral Protein Functions and Comparative Insights from Vaccinia Virus.Animals : an open access journal from MDPI · 2025Review
- Structural dissection of vaccinia G9 identifies residues essential for membrane fusion and complex assembly.Journal of virology · 2025Article
- The 2.3 Å Structure of A21, a Protein Component of the Conserved Poxvirus Entry-Fusion Complex.Journal of molecular biology · 2025Article
- Poxvirus structural biology for application to vaccine design.Trends in immunology · 2025Review
- Temporal expression classes and functions of vaccinia virus and mpox (monkeypox) virus genes.mBio · 2025Review
- Which Proteins? The Challenge of Identifying the Protective Antigens for Next-Generation Capripoxvirus Vaccines.Vaccines · 2025Review
- Japanese encephalitis virus inhibits superinfection of Zika virus in cells by the NS2B protein.Journal of virology · 2024Article
- Development of chimeric antigen receptor (CAR)-T cells targeting A56 viral protein implanted by oncolytic virus.iScience · 2024Article
- Structural and functional analyses of viral H2 protein of the vaccinia virus entry fusion complex.Journal of virology · 2023Article
- Structural basis of poxvirus A16/G9 binding for sub-complex formation.Emerging microbes & infections · 2023Article
- Structural and functional analysis of vaccinia viral fusion complex component protein A28 through NMR and molecular dynamic simulations.PLoS pathogens · 2023Article
- Insights into the Organization of the Poxvirus Multicomponent Entry-Fusion Complex from Proximity Analyses in Living Infected Cells.Journal of virology · 2021Article
- Fusogenic oncolytic vaccinia virus enhances systemic antitumor immune response by modulating the tumor microenvironment.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Loss of the vaccinia virus 35-amino acid hydrophobic O3 protein is partially compensated by mutations in the transmembrane domains of other entry proteins.Journal of virology · 2021Article
- Mutations Near the N Terminus of Vaccinia Virus G9 Protein Overcome Restrictions on Cell Entry and Syncytium Formation Imposed by the A56/K2 Fusion Regulatory Complex.Journal of virology · 2020Article
- Experimental Evolution To Isolate Vaccinia Virus Adaptive G9 Mutants That Overcome Membrane Fusion Inhibition via the Vaccinia Virus A56/K2 Protein Complex.Journal of virology · 2020Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Deletion of the A56R or K2L gene of vaccinia virus (VACV) results in the spontaneous fusion of infected cells to form large multinucleated syncytia. A56 and K2 polypeptides bind to one another (A56/K2) and together are required for interaction with the VACV entry fusion complex (EFC); this association has been proposed to prevent the fusion of infected cells. At least eight viral polypeptides comprise the EFC, but no information has been available regarding their interactions either with each other or with A56/K2. Utilizing a panel of recombinant VACVs designed to repress expression of individual EFC subunits, we demonstrated that A56/K2 interacted with two polypeptides: A16 and G9. Both A16 and G9 were required for the efficient binding of each to A56/K2, suggesting that the two polypeptides interact with each other within the EFC. Such an interaction was established by the copurification of A16 and G9 from infected cells under conditions in which a stable EFC complex failed to assemble and from detergent-treated lysates of uninfected cells that coexpressed A16 and G9. A recombinant VACV that expressed G9 modified with an N-terminal epitope tag induced the formation of syncytia, suggesting partial interference with the functional interaction of A56/K2 with the EFC during infection. These data suggest that A16 and G9 are physically associated within the EFC and that their interaction with A56/K2 suppresses spontaneous syncytium formation and possibly "fuse-back" superinfection of cells.
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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.