ArticlePLoS pathogens2013
Epstein - Barr virus transforming protein LMP-1 alters B cells gene expression by promoting accumulation of the oncoprotein ΔNp73α.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Interactome of the oncogenic ΔNp73α isoform in human papillomavirus 38 E6/E7-transformed keratinocytes.Microbiology resource announcements · 2025Article
- Leaky Artemis Deficiency and EBV-Related Lymphoproliferative Disease: A Novel Case and Review of the Literature.EJHaem · 2025Article
- HPV38 impairs UV-induced transcriptional activation of the IL-18 pro-inflammatory cytokine.mSphere · 2023Article
- Article
- Effect of Epstein-Barr Virus Infection on Selected Immunological Parameters in Children with Type 1 Diabetes.International journal of molecular sciences · 2023Article
- EZH2 abnormalities in lymphoid malignancies: underlying mechanisms and therapeutic implications.Journal of hematology & oncology · 2019Review
- The interplay between Epstein-Bar virus (EBV) with the p53 and its homologs during EBV associated malignancies.Heliyon · 2019Review
- Interplay between the Epigenetic Enzyme Lysine (K)-Specific Demethylase 2B and Epstein-Barr Virus Infection.Journal of virology · 2019Article
- Review
- ZIKV infection effects changes in gene splicing, isoform composition and lncRNA expression in human neural progenitor cells.Virology journal · 2017Article
- The conundrum of the Epstein-Barr virus-associated gastric carcinoma in the Americas.Oncotarget · 2017Review
- Epstein-Barr Virus Oncoprotein LMP1 Mediates Epigenetic Changes in Host Gene Expression through PARP1.Journal of virology · 2016Article
- Epstein-Barr Virus: Diseases Linked to Infection and Transformation.Frontiers in microbiology · 2016Review
- JNK1 Derived from Orange-Spotted Grouper, Epinephelus coioides, Involving in the Evasion and Infection of Singapore Grouper Iridovirus (SGIV).Frontiers in microbiology · 2016Article
- Expression of the epidermodysplasia verruciformis-associated genes EVER1 and EVER2 is activated by exogenous DNA and inhibited by LMP1 oncoprotein from Epstein-Barr virus.Journal of virology · 2015Article
- Epstein-Barr virus down-regulates tumor suppressor DOK1 expression.PLoS pathogens · 2014Article
- Oncoprotein E7 from beta human papillomavirus 38 induces formation of an inhibitory complex for a subset of p53-regulated promoters.Journal of virology · 2013Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many studies have proved that oncogenic viruses develop redundant mechanisms to alter the functions of the tumor suppressor p53. Here we show that Epstein-Barr virus (EBV), via the oncoprotein LMP-1, induces the expression of ΔNp73α, a strong antagonist of p53. This phenomenon is mediated by the LMP-1 dependent activation of c-Jun NH2-terminal kinase 1 (JNK-1) which in turn favours the recruitment of p73 to ΔNp73α promoter. A specific chemical inhibitor of JNK-1 or silencing JNK-1 expression strongly down-regulated ΔNp73α mRNA levels in LMP-1-containing cells. Accordingly, LMP-1 mutants deficient to activate JNK-1 did not induce ΔNp73α accumulation. The recruitment of p73 to the ΔNp73α promoter correlated with the displacement of the histone-lysine N-methyltransferase EZH2 which is part of the transcriptional repressive polycomb 2 complex. Inhibition of ΔNp73α expression in lymphoblastoid cells (LCLs) led to the stimulation of apoptosis and up-regulation of a large number of cellular genes as determined by whole transcriptome shotgun sequencing (RNA-seq). In particular, the expression of genes encoding products known to play anti-proliferative/pro-apoptotic functions, as well as genes known to be deregulated in different B cells malignancy, was altered by ΔNp73α down-regulation. Together, these findings reveal a novel EBV mechanism that appears to play an important role in the transformation of primary B cells.
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