Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA144371 | ENA |
REPOSITORIES: ENA
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Project description:The Epstein-Barr Virus (EBV) Nuclear Antigen 1 (EBNA1) protein is required for the establishment of EBV latent infection in proliferating B-lymphocytes. EBNA1 is a multifunctional DNA-binding protein that stimulates DNA replication at the viral origin of plasmid replication (OriP), regulates transcription of viral and cellular genes, and tethers the viral episome to the cellular chromosome. EBNA1 also provides a survival function to B-lymphocytes, potentially through its ability to alter cellular gene expression. Chromatin-immunoprecipitation (ChIP) combined with massively parallel deep-sequencing (ChIP-Seq) was used to identify cellular sites bound by EBNA1. Sites identified by ChIP-Seq were validated by conventional real-time PCR, and ChIP-Seq provided quantitative, high-resolution detection of the known EBNA1 binding sites on the EBV genome at OriP and Qp. We identified at least one cluster of unusually high-affinity EBNA1 binding sites on chromosome 11, between the divergent FAM55D and FAM55B genes. A consensus for all cellular EBNA1 binding sites is distinct from those derived from the known viral binding sites, suggesting that some of these sites are indirectly bound by EBNA1. We conclude that EBNA1 can interact with a large number of cellular genes and chromosomal loci in latently infected cells, but that these sites are likely to represent a complex ensemble of direct and indirect EBNA1 binding sites. Study of Epstein-Barr virus (EBV)
2011-07-16 | E-GEOD-30709 | biostudies-arrayexpress
Project description:The Epstein-Barr Virus (EBV) Nuclear Antigen 1 (EBNA1) protein is required for the establishment of EBV latent infection in proliferating B-lymphocytes. EBNA1 is a multifunctional DNA-binding protein that stimulates DNA replication at the viral origin of plasmid replication (OriP), regulates transcription of viral and cellular genes, and tethers the viral episome to the cellular chromosome. EBNA1 also provides a survival function to B-lymphocytes, potentially through its ability to alter cellular gene expression. Chromatin-immunoprecipitation (ChIP) combined with massively parallel deep-sequencing (ChIP-Seq) was used to identify cellular sites bound by EBNA1. Sites identified by ChIP-Seq were validated by conventional real-time PCR, and ChIP-Seq provided quantitative, high-resolution detection of the known EBNA1 binding sites on the EBV genome at OriP and Qp. We identified at least one cluster of unusually high-affinity EBNA1 binding sites on chromosome 11, between the divergent FAM55D and FAM55B genes. A consensus for all cellular EBNA1 binding sites is distinct from those derived from the known viral binding sites, suggesting that some of these sites are indirectly bound by EBNA1. We conclude that EBNA1 can interact with a large number of cellular genes and chromosomal loci in latently infected cells, but that these sites are likely to represent a complex ensemble of direct and indirect EBNA1 binding sites.
2011-07-16 | GSE30709 | GEO
Project description:Epstein-Barr virus (EBV) is a ubiquitous gammaherpes virus that establishes a life-long latency in over 90% of the world's population. Epstein Barr Nuclear Antigen 1, EBNA1, is the only viral protein consistently detected in all viral latency programs, as well as in all forms of EBV-associated malignancies. EBNA1 plays critical roles in the viral life cycle by fostering the replication and maintenance of the extrachromosomal viral genome as well as enhancing transcription from multiple viral promoters. Using chromatin immunoprecipitation and human promoter microarrays (an analysis termed ChIP-chip) we found that EBNA1 binds site specifically within multiple human promoters. To determine whether EBNA1’s binding to these promoters perturbed gene expression, we measured the levels of cellular mRNAs by microarrays when EBNA1 was inhibited by a dominant negative derivative of EBNA1 (DomNeg1). Keywords: viral regulation of cellular genes
2009-01-01 | GSE13315 | GEO
Project description:Epstein-Barr virus (EBV) genomes persist in latently infected cells as extrachromosomal plasmids that attach to host chromosomes through the tethering functions of EBNA1, a viral encoded sequence-specific DNA binding protein. Here we employed circular chromosome conformation capture (4C) analysis to identify genomewide associations between EBV episomes and host chromosomes. We found that EBV episomes in Burkitt lymphoma (BL) cells preferentially associate with EBNA1 sequence-specific DNA binding sites in the cellular genome that are also enriched for B-cell factors EBF1 and RBP-jK, the repressive histone mark H3K9me3, and surrounded by AT-rich sequence. These attachment sites corresponded to transcriptionally silenced genes with enrichment in neuronal function. Depletion of EBNA1 from EBV latently infected BL cells led to a transcriptional de-repression of these silenced genes. EBV attachment sites in lymphoblastoid cells (LCLs) showed different correlations, suggesting that latency types are functionally linked to the epigenetic environment of host chromosome attachment sites.
2019-11-14 | GSE129703 | GEO
Project description:Epstein-Barr virus (EBV) is a ubiquitous gammaherpes virus that establishes a life-long latency in over 90% of the world's population. Epstein Barr Nuclear Antigen 1, EBNA1, is the only viral protein consistently detected in all viral latency programs, as well as in all forms of EBV-associated malignancies. EBNA1 plays critical roles in the viral life cycle by fostering the replication and maintenance of the extrachromosomal viral genome as well as enhancing transcription from multiple viral promoters. Using chromatin immunoprecipitation and human promoter microarrays (an analysis termed ChIP-chip) we found that EBNA1 binds site specifically within multiple human promoters. To determine whether EBNA1â??s binding to these promoters perturbed gene expression, we measured the levels of cellular mRNAs by microarrays when EBNA1 was inhibited by a dominant negative derivative of EBNA1 (DomNeg1). Keywords: viral regulation of cellular genes We analysed mRNA expression from the EBV-positive lymphoblastoid cell line 721 transduced with either a control (empty) retroviral vector or a DomNeg1-encoding retroviral vector. For ChIP-chip, DNA from immunoprecipitated chromatin using a anti-EBNA1 antibody (IH4) along with total chromatin was hybridized to a Nimblegen human promoter arrays (CHAR0150-HP2). A single ChIP-chip experiment was performed with DNAs pooled equally from three independent ChIP experiments.
2010-05-14 | E-GEOD-13315 | biostudies-arrayexpress
Project description:Epstein-Barr virus (EBV) is a ubiquitous human ɣ-herpesvirus implicated in various malignancies, including Burkitt’s lymphoma and gastric carcinomas. In most EBV-associated cancers, the viral genome is maintained as an extrachromosomal episome by the EBV nuclear antigen-1 (EBNA1). EBNA1 is considered to be a highly stable protein that interacts with the ubiquitin-specific protease 7 (USP7), but the precise role of USP7 in controlling EBNA1 stability and function is not fully understood. Here, we show that pharmacological inhibitors and small interfering RNA (siRNA) targeting USP7 reduce EBNA1 protein levels. The USP7 inhibitor GNE6776 altered EBNA1 protein interactions, including disrupting its ability to bind to USP7. GNE6776 also inhibited EBNA1 binding to EBV oriP DNA and reduced viral episome copy number. GNE6776 selectively inhibited EBV+ gastric and lymphoid cell proliferation in cell culture and slowed EBV+ tumor growth in mouse xenograft models. Transcriptomic studies revealed that USP7 inhibition differentially affected EBV+ cancer cells compared to EBV- cells with a significant effect on chromosome segregation and mitotic cell division pathways. Our findings indicate that USP7 inhibition perturbs EBNA1 stability and function and can be exploited to target EBV+ cancer cells selectively.
2025-01-31 | GSE284839 | GEO
Project description:Identifying Sites Bound by Epstein Barr Nuclear Antigen 1 (EBNA1) in the Human Genome
| PRJNA109901 | ENA
Project description:We report the application of ChIP Seq to study the Epstein Barr Virus Nuclear Antigen EBNA3A, EBNA3B, EBNA3C, an essential transcriptional regulator involved in the transformation of Resting B Lymphocytes to the immortalized Lymphoblast Cell Lines. Examination of EBNA3A, EBNA3B and EBNA3C protein genome binding in LCLs.
2016-01-05 | E-GEOD-76166 | biostudies-arrayexpress
Project description:RATIONALE: The Epstein Barr virus can cause cancer and lymphoproliferative disorders. Ganciclovir is an antiviral drug that acts against the Epstein Barr virus. Arginine butyrate may make virus cells more sensitive to ganciclovir. Combining ganciclovir and arginine butyrate may kill more Epstein Barr virus cells and tumor cells.
PURPOSE: Phase I trial to study the effectiveness of arginine butyrate plus ganciclovir in treating patients who have cancer or lymphoproliferative disorders that are associated with the Epstein Barr virus.
| 2005372 | ecrin-mdr-crc