GEO series

Regulation of Epstein–Barr Virus latency by histone variant H2A.Z [ChIP-seq]

GSE289711 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 10 samples Submitted 2026/02/13 Platform GPL30173

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 10 samples

What it is: ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism: Homo sapiens (human)
Topic: Burkitt lymphomaThis series is part of our curated briefing on it.
Samples: 10 samples: 10 samples, each with a distinct title — no replicated groupsGroups are read from the sample names, not from the paper. Check the list below.
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.

Summary (written by the submitters)

Chromatin structure plays a central role in the regulation of Epstein-Barr Virus (EBV) latency. The histone variant H2A.Z.1 has been implicated in chromatin structures associated with initiation of transcription and DNA replication. Here, we examined the role of H2AZ.1 in the regulation of EBV chromatin and gene expression during EBV latent infection in two different EBV cancer cell models.

Read the full summary ↓

We found that H2A.Z.1 is highly enriched with EBNA1 binding sites at oriP and Qp, and to a lesser extent with transcriptionally active CTCF binding sites on the EBV genomes in both Mutu I Burkitt lymphoma (BL) and SNU7-19 EBV-associated gastric carcinoma (EBVaGC) cell lines. RNA-interference depletion of H2A.Z.1 resulted in the reactivation of viral lytic genes (ZTA and EAD) and increases viral DNA copy numbers in both MutuI and SNU719 cells. H2A.Z depletion also led to a decrease in EBNA1 binding to oriP and Qp, on the viral episome as well as on plasmids independently of other viral genes and genomes. H2A.Z.1 depletion also reduced peaks of H3K27ac and H4K20me3 at regulatory elements in the EBV genome. In the cellular genome, H2A.Z.1 colocalized with only a subset of EBNA1 binding sites and H2A.Z.1 depletion altered transcription of genes associated with myc targets and mTORC1 signaling. Taken together, these findings indicate that H2A.Z.1 plays an important regulatory role in the regulation of EBNA1 chromatin binding and function in the EBV episome and host chromosome, as well as the epigenetic programming of the latent episome.

This dataset

Open GSE289711 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Burkitt lymphoma landscape →

Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE289711_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1224239 and SRA study SRP564150. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

10 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 10 sample titles: 10 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

GSM8797351 1_Mutu1-EBNA1-A_ChIP
GSM8797352 2_Mutu1-EBNA1-B_ChIP
GSM8797353 3_Mutu1-INPUT_ChIP
GSM8797354 4_Mutu1-H2A.Z-A_ChIP
GSM8797355 5_Mutu1-H2A.Z-B_ChIP
GSM8797356 6_SNU719-EBNA1-A_ChIP
GSM8797357 7_SNU719-EBNA1-B_ChIP
GSM8797358 8_SNU719-INPUT_ChIP
GSM8797359 9_SNU719-H2A.Z-A_ChIP
GSM8797360 10_SNU719-H2A.Z-B_ChIP

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GSE289710 Regulation of Epstein–Barr Virus latency by histone variant H2A.Z [RNA-seq] 6 samples same disease briefing · shares h2a, epstein, latency, histone, variant, virus, barr
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Search all human ChIP / ATAC / CUT&Tag datasets in GEO →

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.