ArticleJournal of virology2012
The lipid raft-associated protein CD98 is required for vaccinia virus endocytosis.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 63 citations in OpenAlex.
- RPSA enhances African swine fever virus entry via caveola-mediated endocytic pathway.Journal of virology · 2026Article
- The macrophage entry mechanism of SARS-CoV-2 mediated by surface CD98/TMPRSS11E complex is associated with the cellular tropism toward proinflammatory M1 and pathogenesis.Respiratory research · 2026Article
- Cellular lipids: fundamental host factors for monkeypox virus replication and pathogenesis.Archives of microbiology · 2026Review
- Methods to Study Poxvirus Structures by Cryo-EM Imaging Modalities.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Structure, Attachment and Transmembrane Internalisation of Peste Des Petits Ruminants Virus.Veterinary medicine and science · 2025Review
- Plant-Derived Vesicle-like Nanoparticles: The Next-Generation Drug Delivery Nanoplatforms.Pharmaceutics · 2024Review
- Myxoma Virus Combination Therapy Enhances Lenalidomide and Bortezomib Treatments for Multiple Myeloma.Pathogens (Basel, Switzerland) · 2024Article
- Repurposing Amphotericin B and Its Liposomal Formulation for the Treatment of Human Mpox.International journal of molecular sciences · 2023Article
- CD98 heavy chain as a prognostic biomarker and target for cancer treatment.Frontiers in oncology · 2023Review
- Identification of β2 microglobulin, the product of B2M gene, as a Host Factor for Vaccinia Virus Infection by Genome-Wide CRISPR genetic screens.PLoS pathogens · 2022Article
- ARF1 with Sec7 Domain-Dependent GBF1 Activates Coatomer Protein I To Support Classical Swine Fever Virus Entry.Journal of virology · 2022Article
- Role of Lipid Rafts in Pathogen-Host Interaction - A Mini Review.Frontiers in immunology · 2021Review
- Membrane Rafts: Portals for Viral Entry.Frontiers in microbiology · 2021Review
- Internalization of Garlic-Derived Nanovesicles on Liver Cells is Triggered by Interaction With CD98.ACS omega · 2020Article
- Tracking Pathogen Infections by Time-Resolved Chemical Proteomics.Angewandte Chemie (International ed. in English) · 2020Article
- Oncolytic Virotherapy with Myxoma Virus.Journal of clinical medicine · 2020Review
- The transporters SLC35A1 and SLC30A1 play opposite roles in cell survival upon VSV virus infection.Scientific reports · 2019Article
- Vaccinia viral A26 protein is a fusion suppressor of mature virus and triggers membrane fusion through conformational change at low pH.PLoS pathogens · 2019Article
- Hepatitis C Virus Modulates Solute carrier family 3 member 2 for Viral Propagation.Scientific reports · 2018Article
- A comparative review of viral entry and attachment during large and giant dsDNA virus infections.Archives of virology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mature vaccinia virus (vaccinia MV) infects a broad range of animals in vivo and cell cultures in vitro; however, the cellular receptors that determine vaccinia MV tropism and entry pathways are poorly characterized. Here, we performed quantitative proteomic analyses of lipid raft-associated proteins upon vaccinia MV entry into HeLa cells. We found that a type II membrane glycoprotein, CD98, is enriched in lipid rafts upon vaccinia MV infection compared to mock-infected HeLa cells. The knockdown of CD98 expression in HeLa cells significantly reduced vaccinia MV entry. Furthermore, CD98 knockout (KO) mouse embryonic fibroblasts (MEFs) also exhibited reduced vaccinia MV infectivity without affecting MV attachment to cells, suggesting a role for CD98 in the postbinding step of virus entry. Further characterization with inhibitors and dominant negative proteins that block different endocytic pathways revealed that vaccinia MV entry into MEFs occurs through a clathrin-independent, caveolin-independent, dynamin-dependent, fluid-phase endocytic pathway, implying that CD98 plays a specific role in the vaccinia MV endocytic pathway. Infections of wild-type and CD98 KO MEF cells with different strains of vaccinia MV provided further evidence that CD98 plays a specific role in MV endocytosis but not in plasma membrane fusion. Finally, different CD98-C69 chimeric proteins were expressed in CD98 KO MEFs, but none were able to reconstitute MV infectivity, suggesting that the overall structure of the CD98 protein is required for vaccinia MV endocytosis.
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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.