ArticleMolecular and cellular biology1999
The amino-terminal C/H1 domain of CREB binding protein mediates zta transcriptional activation of latent Epstein-Barr virus.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 69 citations in OpenAlex.
- A System-Level Perspective on Epstein-Barr Virus Persistence: The Partial Lytic Reactivation.International journal of molecular sciences · 2026Review
- Caspases Switch off the mmBio · 2021Article
- Review
- Ubiquitin Modification of the Epstein-Barr Virus Immediate Early Transactivator Zta.Journal of virology · 2020Article
- Oncogenic Properties of the EBV ZEBRA Protein.Cancers · 2020Review
- A Noncanonical Basic Motif of Epstein-Barr Virus ZEBRA Protein Facilitates Recognition of Methylated DNA, High-Affinity DNA Binding, and Lytic Activation.Journal of virology · 2019Article
- BZLF1 interacts with chromatin remodelers promoting escape from latent infections with EBV.Life science alliance · 2019Article
- Therapeutics Targeting Protein Acetylation Perturb Latency of Human Viruses.ACS chemical biology · 2016Review
- Dynamic Epstein-Barr virus gene expression on the path to B-cell transformation.Advances in virus research · 2014Review
- Viral genome methylation differentially affects the ability of BZLF1 versus BRLF1 to activate Epstein-Barr virus lytic gene expression and viral replication.Journal of virology · 2013Article
- BZLF1 governs CpG-methylated chromatin of Epstein-Barr Virus reversing epigenetic repression.PLoS pathogens · 2012Article
- CpG-methylation regulates a class of Epstein-Barr virus promoters.PLoS pathogens · 2010Article
- A subset of replication proteins enhances origin recognition and lytic replication by the Epstein-Barr virus ZEBRA protein.PLoS pathogens · 2010Article
- Transcriptional repression by sumoylation of Epstein-Barr virus BZLF1 protein correlates with association of histone deacetylase.The Journal of biological chemistry · 2010Article
- Functional interaction between Epstein-Barr virus replication protein Zta and host DNA damage response protein 53BP1.Journal of virology · 2009Article
- Role of chromatin during herpesvirus infections.Biochimica et biophysica acta · 2009Review
- TORC2, a coactivator of cAMP-response element-binding protein, promotes Epstein-Barr virus reactivation from latency through interaction with viral BZLF1 protein.The Journal of biological chemistry · 2009Article
- Histone hyperacetylation occurs on promoters of lytic cycle regulatory genes in Epstein-Barr virus-infected cell lines which are refractory to disruption of latency by histone deacetylase inhibitors.Journal of virology · 2008Article
- Article
- Multivalent sequence recognition by Epstein-Barr virus Zta requires cysteine 171 and an extension of the canonical B-ZIP domain.Journal of virology · 2006Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Latent Epstein-Barr virus (EBV) is maintained as a nucleosome-covered episome that can be transcriptionally activated by overexpression of the viral immediate-early protein, Zta. We show here that reactivation of latent EBV by Zta can be significantly enhanced by coexpression of the cellular coactivators CREB binding protein (CBP) and p300. A stable complex containing both Zta and CBP could be isolated from lytically stimulated, but not latently infected RAJI nuclear extracts. Zta-mediated viral reactivation and transcriptional activation were both significantly inhibited by coexpression of the E1A 12S protein but not by an N-terminal deletion mutation of E1A (E1ADelta2-36), which fails to bind CBP. Zta bound directly to two related cysteine- and histidine-rich domains of CBP, referred to as C/H1 and C/H3. These domains both interacted specifically with the transcriptional activation domain of Zta in an electrophoretic mobility shift assay. Interestingly, we found that the C/H3 domain was a potent dominant negative inhibitor of Zta transcriptional activation function. In contrast, an amino-terminal fragment containing the C/H1 domain was sufficient for coactivation of Zta transcription and viral reactivation function. Thus, CBP can stimulate the transcription of latent EBV in a histone acetyltransferase-independent manner mediated by the CBP amino-terminal C/H1-containing domain. We propose that CBP may regulate aspects of EBV latency and reactivation by integrating cellular signals mediated by competitive interactions between C/H1, C/H3, and the Zta activation domain.
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