ArticleJournal of virology2008
Latent membrane protein 2B regulates susceptibility to induction of lytic Epstein-Barr virus infection.
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 23 papers.
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Who cites it
23 citing papers in PubMed, 49 citations in OpenAlex.
- Proteome-Wide Serological Profiling Reveals Broad Elevation of EBV Immunity in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2026Article
- TNFRSF13B Variant-Induced TACI Dysregulation Underlies CAEBV Pathogenesis.Journal of clinical immunology · 2026Article
- Review
- Carcinogenic mechanisms of virus-associated lymphoma.Frontiers in immunology · 2024Review
- EBV and Lymphomagenesis.Cancers · 2023Review
- Epstein-Barr Virus History and Pathogenesis.Viruses · 2023Review
- Mechanisms of T cell evasion by Epstein-Barr virus and implications for tumor survival.Frontiers in immunology · 2023Review
- Novel EBV LMP-2-affibody and affitoxin in molecular imaging and targeted therapy of nasopharyngeal carcinoma.PLoS pathogens · 2020Article
- The interplay between Epstein-Bar virus (EBV) with the p53 and its homologs during EBV associated malignancies.Heliyon · 2019Review
- Mechanisms of B-Cell Oncogenesis Induced by Epstein-Barr Virus.Journal of virology · 2019Review
- Constructing TC-1-GLUC-LMP2 Model Tumor Cells to Evaluate the Anti-Tumor Effects of LMP2-Related Vaccines.Viruses · 2018Article
- The regulatory network of nasopharyngeal carcinoma metastasis with a focus on EBV, lncRNAs and miRNAs.American journal of cancer research · 2018Review
- Frequency of Epstein Barr Virus Type 1 Among Nasopharyngeal Carcinomas in Iranian PatientsAsian Pacific journal of cancer prevention : APJCP · 2017Article
- Pathogenic Role of Exosomes in Epstein-Barr Virus (EBV)-Associated Cancers.International journal of biological sciences · 2017Review
- IRAK4 is essential for TLR9-induced suppression of Epstein-Barr virus BZLF1 transcription in Akata Burkitt's lymphoma cells.PloS one · 2017Article
- Long and Short Isoforms of the Human Cytomegalovirus UL138 Protein Silence IE Transcription and Promote Latency.Journal of virology · 2016Article
- Epstein-Barr virus latent genes.Experimental & molecular medicine · 2015Review
- The effect of Epstein-Barr virus Latent Membrane Protein 2 expression on the kinetics of early B cell infection.PloS one · 2013Article
- Telomeres and viruses: common themes of genome maintenance.Frontiers in oncology · 2012Article
- Deciphering the role of Epstein-Barr virus in the pathogenesis of T and NK cell lymphoproliferations.Herpesviridae · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The B-lymphotropic Epstein-Barr virus (EBV) encodes two isoforms of latent membrane protein 2 (LMP2), LMP2A and LMP2B, which are expressed during latency in B cells. The function of LMP2B is largely unknown, whereas LMP2A blocks B-cell receptor (BCR) signaling transduction and induction of lytic EBV infection, thereby promoting B-cell survival. Transfection experiments on LMP2B in EBV-negative B cells and the silencing of LMP2B in EBV-harboring Burkitt's lymphoma-derived Akata cells suggest that LMP2B interferes with the function of LMP2A, but the role of LMP2B in the presence of functional EBV has not been established. Here, LMP2B, LMP2A, or both were overexpressed in EBV-harboring Akata cells to study the function of LMP2B. The overexpression of LMP2B increased the magnitude of EBV switching from its latent to its lytic form upon BCR cross-linking, as indicated by a more-enhanced upregulation and expression of EBV lytic genes and significantly increased production of transforming EBV compared to Akata vector control cells or LMP2A-overexpressing cells. Moreover, LMP2B lowered the degree of BCR cross-linking required to induce lytic EBV infection. Finally, LMP2B colocalized with LMP2A as demonstrated by immunoprecipitation and immunofluorescence and restored calcium mobilization upon BCR cross-linking, a signaling process inhibited by LMP2A. Thus, our findings suggest that LMP2B negatively regulates the function of LMP2A in preventing the switch from latent to lytic EBV replication.
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