ArticleJournal of virology2005
The Epstein-Barr virus-encoded LMP2A and LMP2B proteins promote epithelial cell spreading and motility.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed.
- Epstein-Barr Viruses: Their Immune Evasion Strategies and Implications for Autoimmune Diseases.International journal of molecular sciences · 2024Review
- Carcinogenic mechanisms of virus-associated lymphoma.Frontiers in immunology · 2024Review
- Epstein-Barr Virus (EBV) Epithelial Associated Malignancies: Exploring Pathologies and Current Treatments.International journal of molecular sciences · 2022Review
- Review
- The interplay between Epstein-Bar virus (EBV) with the p53 and its homologs during EBV associated malignancies.Heliyon · 2019Review
- Triptolide suppresses the proliferation and induces the apoptosis of nasopharyngeal carcinoma cells via the PI3K/Akt pathway.Oncology letters · 2019Article
- Frequency of Epstein Barr Virus Type 1 Among Nasopharyngeal Carcinomas in Iranian PatientsAsian Pacific journal of cancer prevention : APJCP · 2017Article
- Lentivirus-mediated RNAi knockdown ofExperimental and therapeutic medicine · 2017Article
- Pathogenic Role of Exosomes in Epstein-Barr Virus (EBV)-Associated Cancers.International journal of biological sciences · 2017Review
- Chimerically fused antigen rich of overlapped epitopes from latent membrane protein 2 (LMP2) of Epstein-Barr virus as a potential vaccine and diagnostic agent.Cellular & molecular immunology · 2016Article
- SYK interaction with ITGβ4 suppressed by Epstein-Barr virus LMP2A modulates migration and invasion of nasopharyngeal carcinoma cells.Oncogene · 2015Article
- The role of Epstein-Barr virus infection in the pathogenesis of nasopharyngeal carcinoma.Virologica Sinica · 2015Review
- Understanding the interplay between host immunity and Epstein-Barr virus in NPC patients.Emerging microbes & infections · 2015Review
- Epstein-Barr virus latent genes.Experimental & molecular medicine · 2015Review
- Epstein-Barr virus and nasopharyngeal carcinoma.Chinese journal of cancer · 2014Article
- The Epstein-Barr virus-encoded microRNA MiR-BART9 promotes tumor metastasis by targeting E-cadherin in nasopharyngeal carcinoma.PLoS pathogens · 2014Article
- Epstein-Barr virus latent membrane protein 2A contributes to anoikis resistance through ERK activation.Journal of virology · 2013Article
- The effect of Epstein-Barr virus Latent Membrane Protein 2 expression on the kinetics of early B cell infection.PloS one · 2013Article
- Epstein-Barr virus latent membrane protein-2A induces ITAM/Syk- and Akt-dependent epithelial migration through αv-integrin membrane translocation.Journal of virology · 2012Article
- Epstein-Barr virus latent membrane protein 2A promotes invasion of nasopharyngeal carcinoma cells through ERK/Fra-1-mediated induction of matrix metalloproteinase 9.Journal of virology · 2012Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The frequent expression of latent membrane proteins LMP2A and LMP2B in Epstein Barr virus (EBV)-associated tumors suggests that these proteins play a role in EBV-induced epithelial cell growth transformation. Expression of LMP2A and LMP2B had no effect on the morphology of squamous epithelial cells in monolayer culture, but their expression was associated with an increased capacity to spread and migrate on extracellular matrix. Although the mechanisms by which LMP2A and LMP2B promote cell spreading and motility are unclear, the use of selective pharmacological inhibitors has established a role for tyrosine kinases in this phenotype but ruled out contributions of phosphatidylinositol 3-kinase, extracellular signal-regulated kinase/mitogen-activated protein kinase, and protein kinase C. The ability of LMP2B to induce a phenotype that is virtually indistinguishable from that of LMP2A suggests that regions of the LMP2 protein in addition to the cytosolic amino terminus are capable of inducing phenotypic effects in epithelial cells. Thus, rather than serving to modulate the activity of LMP2A, LMP2B may directly engage signaling pathways to influence epithelial cell behavior such as cell adhesion and motility.
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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.