ArticleJournal of virology2004
Accumulation of cytoplasmic beta-catenin and nuclear glycogen synthase kinase 3beta in Epstein-Barr virus-infected cells.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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
38 citing papers in PubMed, 60 citations in OpenAlex.
- Microbial Signals in Cancer: Dissecting Host-Microbiota-Tumor Interactions and Potential Therapeutic Strategy.MedComm · 2026Review
- A distinct isoform of lymphoid enhancer binding factor 1 (LEF1) epigenetically restricts EBV reactivation to maintain viral latency.PLoS pathogens · 2023Article
- Protein Kinase CK2 and Epstein-Barr Virus.Biomedicines · 2023Review
- Viruses in colorectal cancer.Molecular oncology · 2022Review
- Review
- In silico evidence of de novo interactions between ribosomal and Epstein - Barr virus proteins.BMC molecular and cell biology · 2019Article
- G-Alpha Subunit Abundance and Activity Differentially Regulate β-Catenin Signaling.Molecular and cellular biology · 2019Article
- Molecular Determinants and the Regulation of Human Cytomegalovirus Latency and Reactivation.Viruses · 2018Review
- Interaction of viral oncogenic proteins with the Wnt signaling pathway.Iranian journal of basic medical sciences · 2018Review
- Epstein-Barr virus stably confers an invasive phenotype to epithelial cells through reprogramming of the WNT pathway.Oncotarget · 2018Article
- Regulation of Wnt/β-catenin signaling by herpesviruses.World journal of virology · 2016Review
- Genome-wide identification of expression quantitative trait loci for human telomerase.Medicine · 2016Observational
- Effects of recombinant baculovirus AcMNPV-BmK IT on the formation of early cables and nuclear polymerization of actin in Sf9 cells.Cytotechnology · 2016Article
- 5-Hydroxytryptamine promotes hepatocellular carcinoma proliferation by influencing β-catenin.Molecular oncology · 2016Article
- Fine-Tuning of the RIG-I-Like Receptor/Interferon Regulatory Factor 3-Dependent Antiviral Innate Immune Response by the Glycogen Synthase Kinase 3/β-Catenin Pathway.Molecular and cellular biology · 2015Article
- Article
- Lithium chloride decreases proliferation and migration of C6 glioma cells harboring isocitrate dehydrogenase 2 mutant via GSK-3β.Molecular biology reports · 2014Article
- Cryptosporidium parvum-induced ileo-caecal adenocarcinoma and Wnt signaling in a mouse model.Disease models & mechanisms · 2014Article
- Nuclear export of L-periaxin, mediated by its nuclear export signal in the PDZ domain.PloS one · 2014Article
- Extracellular circulating viral microRNAs: current knowledge and perspectives.Frontiers in genetics · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Epstein-Barr virus (EBV) causes infectious mononucleosis and is associated with cancers in immunocompromised populations. EBV establishes a latent infection and immortalizes and transforms B lymphocytes. Several latent proteins have profound effects on cellular growth, including activation of NF-kappaB, phosphatidylinositol 3'-OH kinase (PI3K) signaling, and notch signaling. Activation of PI3K can affect the activity of beta-catenin, the target of the wnt signaling pathway. Deregulation of beta-catenin is associated with a number of malignancies. To determine if beta-catenin is regulated by EBV infection, EBV-infected cells were examined for beta-catenin levels and localization. beta-Catenin was increased in EBV-positive tumor cell lines compared to EBV-negative lines, in EBV-infected Burkitt's lymphoma cell lines, and in EBV-transformed lymphoblastoid cell lines (LCL). In contrast to wnt signaling, EBV consistently induced the accumulation of beta-catenin in the cytoplasm but not the nucleus. The beta-catenin regulating kinase, glycogen synthase kinase 3beta (GSK3beta), was shown to be phosphorylated and inactivated in EBV-infected lymphocytes. Inactivated GSK3beta was localized to the nucleus of EBV-infected LCL. Neither the cytoplasmic accumulation of beta-catenin nor the nuclear inactivation of GSK3beta was affected by the inhibition of PI3K signaling. These data indicate that latent infection with EBV has unique effects on beta-catenin signaling that are distinct from activation of wnt and independent of its effects on PI3K.
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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.