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Decitabine disrupts EBV genomic epiallele DNA methylation patterns around CTCF binding sites to increase chromatin accessibility and lytic transcription in gastric cancer [ChIP-seq]

ABSTRACT: To investigate the EBV genome after Decitabine treatment by CTCF ChIP-seq

ORGANISM(S): human gammaherpesvirus 4

PROVIDER: GSE234603 | GEO | 2023/08/04

REPOSITORIES: GEO

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Decitabine disrupts EBV genomic epiallele DNA methylation patterns around CTCF binding sites to increase chromatin accessibility and lytic transcription in gastric cancer [RNA]

Project description:To investigate the EBV genome after Decitabine treatment by reduced representation bisulfite sequencing, ATAC-seq, and RNA-seq

2023-08-02 | GSE239767 | GEO

Decitabine disrupts EBV genomic epiallele DNA methylation patterns around CTCF binding sites to increase chromatin accessibility and lytic transcription in gastric cancer [ATAC]

Project description:To investigate the EBV genome after Decitabine treatment by reduced representation bisulfite sequencing, ATAC-seq, and RNA-seq

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Decitabine disrupts EBV genomic epiallele DNA methylation patterns around CTCF binding sites to increase chromatin accessibility and lytic transcription in gastric cancer [RRBS]

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Decitabine disrupts EBV genomic epiallele DNA methylation patterns around CTCF binding sites to increase chromatin accessibility and lytic transcription in gastric cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-14 | GSE234658 | GEO

Decitabine disrupts EBV genomic epiallele DNA methylation patterns around CTCF binding sites to increase chromatin accessibility and lytic transcription in gastric cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

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Proteomics of EBV-infected lytic and refractory cells

Project description:Most humans are infected with Epstein-Barr virus (EBV), a cancer-causing virus. While EBV generally persists silently in B lymphocytes, periodic lytic (re-)activation of latent virus is central to its life cycle and to most EBV-related diseases. However, a substantial fraction of EBV-infected B cells and tumor cells in a population is refractory to lytic activation. This resistance to lytic activation directly and profoundly impacts viral persistence and effectiveness of oncolytic therapy for EBV+ cancers. To identify the mechanisms that underlie susceptibility to EBV-lytic activation, we used host protein-expression profiling of separated-lytic and -refractory cells.

2016-04-27 | PXD001838 | Pride

Proteomics of EBV-infected lytic and refractory cells

2016-07-22 | MSV000079993 | MassIVE

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

The Nucleic Acid Binding Protein SFPQ Represses EBV Lytic Reactivation by Promoting Histone H1 Expression

Project description:Epstein-Barr virus (EBV) uses a biphasic lifecycle of latency and lytic reactivation to infect >95% of adults worldwide. Despite its central role in EBV persistence and oncogenesis, much remains unknown about how EBV latency is maintained. We used a human genome-wide CRISPR/Cas9 screen to identify that the nuclear protein SFPQ was critical for latency. SFPQ supported expression of linker histone H1, which stabilizes nucleosomes and regulates nuclear architecture, but has not been previously implicated in EBV gene regulation. H1 occupied latent EBV genomes, including the immediate early gene BZLF1 promoter. Upon reactivation, SFPQ was sequestered into sub-nuclear puncta, and EBV genomic H1 occupancy diminished. Enforced H1 expression blocked EBV reactivation upon SFPQ knockout, confirming it as necessary downstream of SFPQ. SFPQ knockout triggered reactivation of EBV in B and epithelial cells as well as in Kaposi’s Sarcoma Associated Herpesvirus, suggesting a conserved gamma-herpesvirus role. These findings highlight SFPQ as a major regulator of H1 expression and EBV latency.

2024-04-16 | GSE235265 | GEO

Understanding differential expression of genes during EBV lytic cycle reactivation by employing high throughput RNA-sequencing

Project description:To understand the changes in global transcriptomic landscape during the EBV lytic cycle reactivation from lymphoblastoid cell lines (LCLs), RNA-seq was performed. By examining the transcriptomic changes, we obtained valuable insights into the molecular events and regulatory mechanisms involved in EBV reactivation into lytic cycle replication. The study also enhances our knowledge of the complex interplay between EBV and the host cells during its lytic cycle.

2023-08-03 | GSE237484 | GEO

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