ArticleBlood2007
Epstein-Barr virus latent membrane protein 2A is a B-cell receptor mimic and essential for B-cell survival.
Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers.
What it found
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Who cites it
135 citing papers in PubMed, 247 citations in OpenAlex.
- A role for the protease MALT1 in EBV-mediated B-cell transformation by Latent Membrane Proteins 1 and 2.Leukemia · 2026Article
- Limitations of EBV transformed human Raji B cells as a model for measuring canonical NF-κB activation.bioRxiv : the preprint server for biology · 2026Article
- Epstein-Barr virus (EBV) infection causes human germinal center B cell-derived lymphomas in the absence of EBNA2 expression.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A Murine Database of Structural Variants Identifies A Candidate Gene for a Spontaneous Murine Lymphoma Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Epstein-Barr virus-associated tumors: commonalities in pathogenesis and the tumor immune microenvironment.Frontiers in immunology · 2026Review
- Epstein-Barr virus: biology, pathogenesis and therapy of lymphomas.Discover oncology · 2025Review
- Epstein-Barr virus-infected tonsillar marginal zone B cellsJournal of virology · 2025Article
- EBV Latency Programs: Molecular and Epigenetic Regulation and Its Role in Disease Pathogenesis.Journal of medical virology · 2025Review
- Distinct epigenetic and transcriptional profiles of Epstein-Barr virus-positive and negative primary CNS lymphomas.Neuro-oncology · 2025Article
- A Murine Database of Structural Variants Enables the Genetic Architecture of a Spontaneous Murine Lymphoma to be Characterized.bioRxiv : the preprint server for biology · 2025Article
- Differential antibody response to EBV proteome following EBVST immunotherapy in EBV-associated lymphomas.Blood advances · 2025Article
- Observations on seasonal occurrence in lymphomas with proven or presumed infectious etiology.Frontiers in oncology · 2025Article
- B Cell Differentiation and the Origin and Pathogenesis of Human B Cell Lymphomas.Methods in molecular biology (Clifton, N.J.) · 2025Review
- The Functional Interaction Between Epstein-Barr Virus and MYC in the Pathogenesis of Burkitt Lymphoma.Cancers · 2024Review
- Hemophagocytic lymphohistiocytosis: current treatment advances, emerging targeted therapy and underlying mechanisms.Journal of hematology & oncology · 2024Review
- How Epstein Barr Virus Causes Lymphomas.Viruses · 2024Review
- Review
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- EBV-specific T-cell immunity: relevance for multiple sclerosis.Frontiers in immunology · 2024Review
- A Mouse Model to Study the Pathogenesis of γ-herpesviral Infections in Germinal Center B Cells.Cells · 2023Article
75 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Many cells latently infected with Epstein-Barr virus (EBV), including certain virus-associated tumors, express latent membrane protein 2A (LMP2A), suggesting an important role for this protein in viral latency and oncogenesis. LMP2A mimics B-cell receptor signaling but can also act as a decoy receptor blocking B-cell receptor (BCR) activation. Studies of peripheral B cells have not resolved this apparent contradiction because LMP2A seems to be dispensable for EBV-induced transformation of these B cells in vitro. We show here that LMP2A is essential for growth transformation of germinal center B cells, which do not express the genuine BCR because of deleterious somatic hypermutations in their immunoglobulin genes. BCR-positive (BCR(+)) and BCR-negative (BCR(-)) B cells are readily transformed with a recombinant EBV encoding a conditional, floxed LMP2A allele, but the survival and continued proliferation of both BCR(+) and BCR(-) B cells is strictly dependent on LMP2A. These findings indicate that LMP2A has potent, distinct antiapoptotic and/or transforming characteristics and point to its role as an indispensable BCR mimic in certain B cells from which human B-cell tumors such as Hodgkin lymphoma originate.
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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.