ArticleJournal of virology2012
The latent membrane protein 1 (LMP1) oncogene of Epstein-Barr virus can simultaneously induce and inhibit apoptosis in B cells.
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 54 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 84 citations in OpenAlex.
- A System-Level Perspective on Epstein-Barr Virus Persistence: The Partial Lytic Reactivation.International journal of molecular sciences · 2026Review
- Molecular mechanisms of Epstein-Barr Virus in the pathogenesis of lymphomas and new opportunities for precision medicine.Discover oncology · 2026Review
- Epstein-Barr virus LMP1 promotes tumorigenesis in a murine epithelial tumor model.Biochemistry and biophysics reports · 2025Article
- Multifocal osteochondromatous proliferation and paraneoplastic hematologic dyscrasia in the context of latent Epstein-Barr virus reactivation: a case of oncologic and infectious pathophysiology.Skeletal radiology · 2025Article
- Oral hairy leukoplakia: The role of Epstein-Barr virus, the occurrence in immunocompetent patients, and the malignant transformation potential.Journal of dental sciences · 2025Review
- Epstein-Barr virus infection promotes T cell dysregulation in a humanized mouse model of multiple sclerosis.Science advances · 2025Article
- In Silico Modeling and Characterization of Epstein-Barr Virus Latent Membrane Protein 1 Protein.ACS omega · 2024Article
- The Research Progress on Immortalization of Human B Cells.Microorganisms · 2023Review
- LMP1 and EBNA2 constitute a minimal set of EBV genes for transformation of human B cells.Frontiers in immunology · 2023Article
- Malignancy and viral infections in Sub-Saharan Africa: A review.Frontiers in virology (Lausanne, Switzerland) · 2023Article
- The Role of Epstein-Barr Virus in Modulating Key Tumor Suppressor Genes in Associated Malignancies: Epigenetics, Transcriptional, and Post-Translational Modifications.Biomolecules · 2022Review
- Epstein-Barr Virus in Burkitt Lymphoma in Africa Reveals a Limited Set of Whole Genome andFrontiers in oncology · 2022Article
- Proteomic approaches to investigate gammaherpesvirus biology and associated tumorigenesis.Advances in virus research · 2021Review
- Epstein-Barr Virus Limits the Accumulation of IPO7, an Essential Gene Product.Frontiers in microbiology · 2021Article
- Viral MicroRNAs: Interfering the Interferon Signaling.Current pharmaceutical design · 2020Review
- Review
- Interactions between Autophagy and DNA Viruses.Viruses · 2019Review
- Epstein-Barr Virus and Innate Immunity: Friends or Foes?Microorganisms · 2019Review
- Preservation of circadian rhythms by the protein folding chaperone, BiP.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- LMP1 and 2A Induce the Expression of Nrf2 Through Akt Signaling Pathway in Epstein-Barr Virus-Transformed B Cells.Translational oncology · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The latent membrane protein 1 (LMP1) of Epstein-Barr virus (EBV) regulates its own expression and the expression of human genes via its two functional moieties; the transmembrane domains of LMP1 are required to regulate its expression via the unfolded protein response (UPR) and autophagy in B cells, and the carboxy-terminal domain of LMP1 activates cellular signaling pathways that affect cellular proliferation and survival. An apparent anomaly in the complex regulation of the UPR and autophagy by LMP1 is that the induction of either pathway can lead to cellular death, yet neither EBV-infected B cells nor B cells expressing only LMP1 die. Thus, we sought to understand how B cells that express LMP1 survive. The transmembrane domains of LMP1 activated apoptosis in B cells, the apoptosis required the UPR, and the carboxy-terminal domain of LMP1 blocked this apoptosis. The expression of the mRNA of Bcl2a1, encoding an antiapoptotic homolog of BCL2, correlated directly with the expression of LMP1 in EBV-positive B-cell strains, and its expression inhibited the apoptosis induced by the transmembrane domains of LMP1. These findings illustrate how the carboxy-terminal domain of LMP1 supports survival of B cells in the presence of the deleterious effects of the complex regulation of this viral oncogene.
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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.