ArticleThe Journal of biological chemistry2008
Tumor-derived variants of Epstein-Barr virus latent membrane protein 1 induce sustained Erk activation and c-Fos.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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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Who cites it
24 citing papers in PubMed, 45 citations in OpenAlex.
- EBV Genome Variations and Association With Diseases.Journal of medical virology · 2026Review
- Incorporation of Epstein-Barr viral variation implicates significance of Latent Membrane Protein 1 in survival prediction and prognostic subgrouping in Burkitt lymphoma.International journal of cancer · 2025Article
- Mutations in latent membrane protein 1 of Epstein-Barr virus are associated with increased risk of posttransplant lymphoproliferative disorder in children.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2023Article
- Treatment Advances in EBV Related Lymphoproliferative Diseases.Frontiers in oncology · 2022Review
- Biomarkers for PTLD diagnosis and therapies.Pediatric nephrology (Berlin, Germany) · 2020Review
- Molecular characterization of Epstein-Barr virus variants detected in the oral cavity of adolescents in Cali, ColombiaBiomedica : revista del Instituto Nacional de Salud · 2020Article
- Capn4 is induced by and required for Epstein-Barr virus latent membrane protein 1 promotion of nasopharyngeal carcinoma metastasis through ERK/AP-1 signaling.Cancer science · 2020Article
- Human DNA Virus Exploitation of the MAPK-ERK Cascade.International journal of molecular sciences · 2019Review
- Metagenomic analysis of DNA viruses from posttransplant lymphoproliferative disorders.Cancer medicine · 2019Article
- Epstein-Barr Virus Latent Membrane Protein 1 Regulates Host B Cell MicroRNA-155 and Its Target FOXO3aFrontiers in microbiology · 2019Article
- Viral-Targeted Strategies Against EBV-Associated Lymphoproliferative Diseases.Frontiers in oncology · 2019Review
- Therapeutic Strategies against Epstein-Barr Virus-Associated Cancers Using Proteasome Inhibitors.Viruses · 2017Review
- Epstein-Barr Virus Oncoprotein LMP1 Mediates Epigenetic Changes in Host Gene Expression through PARP1.Journal of virology · 2016Article
- Epstein-Barr virus-associated lymphoepithelial carcinoma after pediatric liver transplant.Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society · 2016Article
- The Role of Gammaherpesviruses in Cancer Pathogenesis.Pathogens (Basel, Switzerland) · 2016Review
- Epstein-Barr virus infection induces indoleamine 2,3-dioxygenase expression in human monocyte-derived macrophages through p38/mitogen-activated protein kinase and NF-κB pathways: impairment in T cell functions.Journal of virology · 2014Article
- The interplay between Epstein-Barr virus and B lymphocytes: implications for infection, immunity, and disease.Immunologic research · 2014Review
- SPLUNC1 regulates cell progression and apoptosis through the miR-141-PTEN/p27 pathway, but is hindered by LMP1.PloS one · 2013Article
- Epstein-barr virus sequence variation-biology and disease.Pathogens (Basel, Switzerland) · 2012Review
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Latent membrane protein 1 (LMP1) of Epstein-Barr virus (EBV) is a proven oncogene that is essential for transformation of human B cells by the virus. LMP1 induces constitutive activation of several signal transduction pathways involving nuclear factor kappaB, phosphatidylinositol 3-kinase/Akt, and the mitogen-activated protein kinases (MAPK) p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (Erk). Sequencing of LMP1 isolated from a panel of EBV+ B cell lymphomas identified three different variants of LMP1, each distinct from the B95.8 prototype isoform. All tumor variants of LMP1 as well as the B95.8 LMP1 isoform were able to induce rapid p38 phosphorylation as well as Akt and JNK activation. Additionally all variants showed similar ability to activate nuclear factor kappaB. In contrast, only tumor-derived LMP1 variants induced prolonged Erk activation and c-Fos expression. Sequence analysis revealed only two amino acids, 212 and 366, shared by the tumor variants but distinct from B95.8. Point mutation of either amino acids 212 (glycine to serine) or 366 (serine to threonine) from the B95.8 isoform to the tumor variant version of LMP1 was sufficient for gain of function characterized by sustained activation of Erk and subsequent c-Fos induction and binding to the AP1 site. Our results indicate that the enhanced ability of tumor-derived LMP1 to induce and stabilize the c-Fos oncogene can be localized to two amino acids in the C terminus of LMP1.
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Registered trials
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