ArticleVirus genes2010
Roles of TRAF2 and TRAF3 in Epstein-Barr virus latent membrane protein 1-induced alternative NF-kappaB activation.
Article in Virus genes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Role of Viral Infections in Testicular Cancer Etiology: Evidence From a Systematic Review and Meta-Analysis.Frontiers in endocrinology · 2019Pooled it
- Epstein-barr virus latent membrane protein 1 targets cIAP1, cIAP2 and TRAF2 for proteasomal degradation to activate the non-canonical NF-κB pathway.PLoS pathogens · 2026Article
- Epstein-Barr Virus Latent Membrane Protein 1 targets cIAP1, cIAP2 and TRAF2 for Proteasomal Degradation to Activate the Non-canonical NF-κB Pathway.bioRxiv : the preprint server for biology · 2025Article
- Cancers associated with human gammaherpesviruses.The FEBS journal · 2022Review
- CRISPR-Cas9 Genetic Analysis of Virus-Host Interactions.Viruses · 2018Review
- Epstein-Barr Virus LMP1-Mediated Oncogenicity.Journal of virology · 2017Review
- LHBs can elevate the expression of MDR1 through HIF-1α in patients with CHB infection: a comparative proteomic study.Oncotarget · 2017Article
- The Role of Dendritic Cell Maturation in the Induction of Insulin-Dependent Diabetes Mellitus.Frontiers in immunology · 2017Review
- Burkholderia pseudomallei-derived miR-3473 enhances NF-κB via targeting TRAF3 and is associated with different inflammatory responses compared to Burkholderia thailandensis in murine macrophages.BMC microbiology · 2016Article
- Chimeric Vaccine Stimulation of Human Dendritic Cell Indoleamine 2, 3-Dioxygenase Occurs via the Non-Canonical NF-κB Pathway.PloS one · 2016Article
- ROS and ROS-Mediated Cellular Signaling.Oxidative medicine and cellular longevity · 2016Review
- EBV and human cancer.Experimental & molecular medicine · 2015Article
- Biallelic loss-of-function mutation in NIK causes a primary immunodeficiency with multifaceted aberrant lymphoid immunity.Nature communications · 2014Article
- Epstein-Barr virus-encoded BARF1 promotes proliferation of gastric carcinoma cells through regulation of NF-κB.Journal of virology · 2013Article
- Review
- Parthenolide induces apoptosis and lytic cytotoxicity in Epstein-Barr virus-positive Burkitt lymphoma.Molecular medicine reports · 2012Article
- Microbiome and malignancy.Cell host & microbe · 2011Review
- Modulation of NF-κB signalling by microbial pathogens.Nature reviews. Microbiology · 2011Review
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 at 2 institutions in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1)-induced NF-kappaB activation is essential for EBV-transformed B cell survival. LMP1 has two C-terminal cytoplasmic domains referred to as C-Terminal Activation Regions (CTAR) 1 and 2 that activate the alternative and canonical NF-kappaB pathways, respectively. While CTAR2 activates TRAF6, IKKbeta and IKKgamma-dependent canonical NF-kappaB pathway, CTAR1 interacts with TRAF2 and TRAF3 and activates NIK and IKKalpha-dependent alternative NF-kappaB pathway involving p100 processing into functional p52. Using IKKalpha(-/-), IKKbeta(-/-), IKKgamma(-/-), TRAF2(-/-), TRAF3(-/-), TRAF6(-/-), and NIK(aly/aly) mouse embryonic fibroblasts (MEFs), potential roles of these proteins in LMP1-induced alternative NF-kappaB activation were investigated. Deficiency in IKKalpha or functional NIK, but not in IKKbeta, IKKgamma, or TRAF6, severely impaired LMP1-induced p100 processing. Notably, p100 was constitutively processed in TRAF2(-/-) or TRAF3(-/-) MEFs independently of LMP1 suggesting that TRAF2 or TRAF3 may play a regulatory role in p100 processing. Subsequently, TRAF2 or TRAF3 over-expression in HEK293 cells significantly blocked LMP1-induced p100 processing. The LMP1 CTAR1 expression in 293HEK cells activated the alternative p65/p52 complex while CTAR2 failed to do so. Taken together, LMP1 activates alternative NF-kappaB pathway through functional NIK and IKKalpha that is regulated by TRAF2 or TRAF3.
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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.