ArticleJournal of virology2002
The metastatic suppressor Nm23-H1 interacts with EBNA3C at sequences located between the glutamine- and proline-rich domains and can cooperate in activation of transcription.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Pooled it
- IRX1 suppresses breast cancer progression by inhibiting fatty acid de novo synthesis through downregulating ACACA expression.Cell death & disease · 2026Article
- Exploring EBNA3C Genetic Variability and Recombination in Epstein-Barr Virus-Associated Cancers.International journal of molecular sciences · 2026Article
- Nm23-H1 induces apoptosis in primary effusion lymphoma cells via inhibition of NF-κB signaling through interaction with oncogenic latent protein vFLIP K13 of Kaposi's sarcoma-associated herpes virus.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Negative Effect of Reduced NME1 Expression on Recurrence-Free Survival in Early Stage Non-Small Cell Lung Cancer.Journal of clinical medicine · 2020Article
- Genomic variations in EBNA3C of EBV associate with posttransplant lymphoproliferative disorder.JCI insight · 2020Article
- Metastasis Suppressor NME1 Directly Activates Transcription of theAnticancer research · 2018Article
- Oncogenic Epstein-Barr virus recruits Nm23-H1 to regulate chromatin modifiers.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- NM23/NDPK proteins in transcription regulatory functions and chromatin modulation: emerging trends.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Nuclear functions of NME proteins.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Role of EBNA-3 Family Proteins in EBV Associated B-cell Lymphomagenesis.Frontiers in microbiology · 2016Review
- Dissecting the contribution of EBNA3C domains important for EBV-induced B-cell growth and proliferation.Oncotarget · 2015Article
- EBNA3C regulates p53 through induction of Aurora kinase B.Oncotarget · 2015Article
- The ubiquitin E3 ligase SCF-FBXO24 recognizes deacetylated nucleoside diphosphate kinase A to enhance its degradation.Molecular and cellular biology · 2015Article
- Regulation of the metastasis suppressor Nm23-H1 by tumor viruses.Naunyn-Schmiedeberg's archives of pharmacology · 2015Review
- EBNA3C augments Pim-1 mediated phosphorylation and degradation of p21 to promote B-cell proliferation.PLoS pathogens · 2014Article
- Impact of EBV essential nuclear protein EBNA-3C on B-cell proliferation and apoptosis.Future microbiology · 2013Review
- Nucleoside-diphosphate-kinase: a pleiotropic effector in microbial colonization under interdisciplinary characterization.Microbes and infection · 2012Review
- E2F1 mediated apoptosis induced by the DNA damage response is blocked by EBV nuclear antigen 3C in lymphoblastoid cells.PLoS pathogens · 2012Article
- Review
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 1 institution in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) is a lymphotrophic herpesvirus infecting most of the world's population. It is associated with a number of human lymphoid and epithelial tumors and lymphoproliferative diseases in immunocompromised patients. Recent studies have shown an in vitro and in vivo interaction between the EBV nuclear antigen 3C (EBNA3C) and the metastatic suppressor Nm23-H1, known to be downregulated in human invasive breast carcinoma. In this study, we have identified the domain of EBNA3C that specifically binds to Nm23-H1. This domain lies within the region comprising amino acids 637 to 675 of EBNA3C flanked by the proline- and glutamine-rich domains. Furthermore, we show that Nm23-H1 activates transcription when fused to the Gal4 DNA-binding domain and is coexpressed with a luciferase reporter construct containing the Gal4 binding sites upstream of a basal promoter. Gal4-Nm23-H1, when tethered to the promoter by binding to the Gal4 DNA binding sequences, consistently activated transcription. The level of activation increased when increasing amounts of Gal4-Nm23-H1 were introduced into the system. Moreover, EBNA3C when cotransfected with Gal4-Nm23-H1 enhanced the transcriptional activity. These results suggest that Nm23-H1 may have intrinsic transcription activities in EBV-infected cells and that this activity can be modulated in the presence of the essential latent antigen EBNA3C.
Indexed as
Identifiers
What OpenQuestion holds
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.