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JQ1 prevents BRD4 recruitment to the lytic origins of replication [Akata-Zta DNA-seq]

ABSTRACT: JQ1 prevents BRD4 recruitment to the lytic origins of replication [Akata-Zta DNA-seq]

OTHER RELATED OMICS DATASETS IN: GSE84209GSE84212GSE84213GSE84210GSE84214GSE84211GSE98772GSE98773

PROVIDER: PRJNA386166 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5525950.fastq.gz	Fastqsanger.gz
	SRR5525951.fastq.gz	Fastqsanger.gz
	SRR5525952.fastq.gz	Fastqsanger.gz
	SRR5525953.fastq.gz	Fastqsanger.gz
	SRR5525954.fastq.gz	Fastqsanger.gz

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Similar Datasets

JQ1 prevents BRD4 recruitment to the lytic origins of replication [Akata-Zta Brd4 ChIP-seq]

Project description:JQ1 prevents BRD4 recruitment to the lytic origins of replication [Akata-Zta Brd4 ChIP-seq]

| PRJNA386167 | ENA

JQ1 prevents BRD4 recruitment to the lytic origins of replication [Akata-Zta Brd4 ChIP-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The ChIP-seq data below show that the BET proteins bind to both EBV lytic origins of replication.

2017-06-30 | GSE98773 | GEO

JQ1 prevents BRD4 recruitment to the lytic origins of replication [Akata-Zta DNA-seq]

2017-06-30 | GSE98772 | GEO

BET inhibitors suppress lytic DNA replication [Akata-Zta RNA-seq]

Project description:BET inhibitors suppress lytic DNA replication [Akata-Zta RNA-seq]

| PRJNA328406 | ENA

BET inhibitors suppress lytic DNA replication [Akata-Zta DNA-seq]

Project description:BET inhibitors suppress lytic DNA replication [Akata-Zta DNA-seq]

| PRJNA328410 | ENA

BET inhibitors suppress lytic DNA replication [Akata-Zta DNA-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The sequenced total DNA data below show that JQ1 and I-BET cause a decrease in EBV genome replication after induction.

2017-06-30 | GSE84212 | GEO

BET inhibitors suppress lytic DNA replication [Akata-Zta RNA-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The RNA-seq data below show that the second block causes a decrease in expression of late but not early lytic genes.

2017-06-30 | GSE84211 | GEO

¬¬Identifying the cellular interactome of Epstein-Barr virus lytic regulator Zta reveals cellular targets contributing to viral replication.

Project description:The human gamma herpesvirus Epstein-Barr virus, infects most adults and is an important contributor to the development of many types of cancer. Essential contributions of viral genes to replication are known but the potential contributions of cell genes to viral replication are less well delineated. A key player is the viral protein Zta (BZLF1, ZEBRA, Z). This sequence-specific DNA-binding protein can disrupt viral latency by driving the transcription of target genes and by interacting with the EBV lytic origin of replication. Here we used an unbiased approach to identify the Zta-interactome in cells derived from a Burkitt’s lymphoma. Isolating Zta and associated proteins from Burkitt’s lymphoma cells undergoing EBV replication, followed by Tandem Mass Tag (TMT) mass spectrometry resulted in the identification of forty-four viral and cellular proteins in the Zta interactome. Of these two were known targets of Zta. The association of Zta with Hsc70 and the contribution that Hsc70 plays to EBV replication mirrors a contribution from HSP70 family members to the replication of other herpesviruses. Conversely, the association of Zta with NFATc2 has no known parallels for other herpesviruses. Zta attenuates the activity of an NFAT-dependent promoter, which shows a potential for dampening the expression of genes regulated by calcium-dependent signal transduction. Indeed, Zta has the ability to affect a feed-back loop limiting its own expression, which would aid viral replication by preventing the toxic effects of Zta overexpression.

2019-06-06 | PXD013727 | Pride

Effect of Effect of lytic replication on EBV and cell gene expression

Project description:The effect of Epstein Barr virus replication on cellular gene expression was studied using AGSiZ epithelial cells which are derived from a gastric carcinoma. The cell line is infected with a recombinant strain of EBV known as Akata BX-1. The cell line was further stably transduced with an inducible EBV Zta transactivator gene. When cells are treated with doxycycline, robust lytic replication of EBV is achieved. Cells made permissive for lytic replication in this manner were harvested for RNA suitable for deep sequencing at 24 and 48 hours post induction in parallel with cells that were mock induced with doxycycline to serve as a control for cells not undergoing EBV replication.

2021-04-15 | GSE155811 | GEO

Binding site identification for the Epstein-Barr virus transcription factor Zta in epithelial cells

Project description:Epstein-Barr virus (EBV) is present in a state of latency in infected memory B-cells and EBV-associated lymphoid and epithelial cancers. Cell stimulation or differentiation of infected B-cells and epithelial cells induces reactivation to the lytic replication cycle. In each cell type, the EBV transcription and replication factor Zta (BZLF1, EB1) plays a role in mediating the lytic cycle of EBV. Zta is a transcription factor that interacts directly with Zta response elements (ZREs) within viral and cellular genomes. Here we undertake chromatin-precipitation coupled to DNA-sequencing (ChIP-Seq) of Zta-associated DNA from cancer-derived epithelial cells. The analysis identified over 14,000 Zta-binding sites in the cellular genome. We assessed the impact of lytic cycle reactivation on changes in gene expression for a panel of Zta-associated cellular genes. Finally, we compared the Zta-binding sites identified in this study with those previously identified in B-cells and reveal substantial conservation in genes associated with Zta-binding sites.

2021-02-20 | GSE83354 | GEO

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