ArticleJournal of virology1999
Genetic dissection of cell growth arrest functions mediated by the Epstein-Barr virus lytic gene product, Zta.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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Who cites it
36 citing papers in PubMed, 61 citations in OpenAlex.
- E2F1 suppresses Epstein-Barr virus lytic reactivation through cellular and viral transcriptional networks.PLoS pathogens · 2025Article
- Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.PLoS pathogens · 2024Article
- Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.bioRxiv : the preprint server for biology · 2024Article
- The nucleic acid binding protein SFPQ represses EBV lytic reactivation by promoting histone H1 expression.Nature communications · 2024Article
- Synthetic BZLF1-targeted transcriptional activator for efficient lytic induction therapy against EBV-associated epithelial cancers.Nature communications · 2024Article
- ATM, KAP1 and the Epstein-Barr virus polymerase processivity factor direct traffic at the intersection of transcription and replication.Nucleic acids research · 2023Article
- GJournal of virology · 2022Article
- Ubiquitin Modification of the Epstein-Barr Virus Immediate Early Transactivator Zta.Journal of virology · 2020Article
- The bZIP Proteins of Oncogenic Viruses.Viruses · 2020Review
- Viral-Targeted Strategies Against EBV-Associated Lymphoproliferative Diseases.Frontiers in oncology · 2019Review
- Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.Cell death & disease · 2016Article
- BZLF1 Attenuates Transmission of Inflammatory Paracrine Senescence in Epstein-Barr Virus-Infected Cells by Downregulating Tumor Necrosis Factor Alpha.Journal of virology · 2016Article
- Identification of herpesvirus proteins that contribute to G1/S arrest.Journal of virology · 2014Article
- Cell cycle regulation during viral infection.Methods in molecular biology (Clifton, N.J.) · 2014Review
- Kaposi's sarcoma-associated herpesvirus transactivator Rta induces cell cycle arrest in G0/G1 phase by stabilizing and promoting nuclear localization of p27kip.Journal of virology · 2013Article
- Characterization of the cell-penetrating properties of the Epstein-Barr virus ZEBRA trans-activator.The Journal of biological chemistry · 2010Article
- Initiation of lytic DNA replication in Epstein-Barr virus: search for a common family mechanism.Future virology · 2010Article
- Functional interaction between Epstein-Barr virus replication protein Zta and host DNA damage response protein 53BP1.Journal of virology · 2009Article
- Reactivation of the Epstein-Barr virus from viral latency by an S-adenosylhomocysteine hydrolase/14-3-3 zeta/PLA2-dependent pathway.Medical microbiology and immunology · 2006Article
- Contribution of C/EBP proteins to Epstein-Barr virus lytic gene expression and replication in epithelial cells.Journal of virology · 2006Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Expression of the Epstein-Barr virus (EBV) latency-associated genes activates cell cycle progression and drives immortalization of the infected cell. In contrast, progression of the EBV replication program occurs most efficiently in growth-arrested cells. Previous studies showed that the EBV-encoded immediate-early transcription factor, Zta, can induce expression of the cyclin-dependent kinase inhibitors, p21 and p27, the tumor suppressor, p53, and cell growth arrest. Moreover, Zta-mediated induction of growth arrest occurs independently of its transcriptional transactivation function. Here we show that substitution of Zta's basic DNA binding domain with the analogous region of the Zta homologue, c-Fos, abrogates Zta's ability to induce growth arrest and to induce p21, p27, or p53 expression, suggesting that protein-protein interactions between this region of Zta and key cell cycle control proteins are involved in signaling cell cycle arrest. We also show that despite the crucial role for Zta's basic domain in eliciting cell growth arrest, its amino terminus is required for efficient induction of p27 and it modulates the level of p53 induction. Last, we provide evidence that Zta-mediated inductions of p21, p27, and p53 occur, at least in part, through distinct pathways. Therefore, Zta interacts with multiple growth arrest pathways, a property which may have evolved partly as a means to ensure that lytic replication occurs in a growth-arrested setting in multiple different tissues in various states of differentiation.
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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.