GEO series

Disruption of histone acetylation homeostasis reveals multilayered chromatin regulation for transcriptional resiliency

GSE282758 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2025/10/30 Platform GPL30173

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 12 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)
Samples: 12 samples: 3 × 24hr Control ATAC-seq vs 3 × 24hr SAHA Treated ATAC-seq vs 3 × 48hr Control ATAC-seq vs 3 × 48hr SAHA Treated ATAC-seqGroups 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.
Paper: Disruption of histone acetylation homeostasis reveals multilayered chromatin regulation for transcriptional resiliencyEpigenetics & chromatin · 2025

Summary (written by the submitters)

Dysregulation of epigenetic processes leads to a plethora of abnormalities including disease states such as cancer. Therapies focused on epigenetic modulation alter gene expression to correct dysfunction, though the mechanisms and perpetuation of these states is unknown. Here, we use integrated epigenomics and three-dimensional chromatin structure-function analyses after acute histone deacetylase inhibitor cancer drug treatment (suberoylanilide hydroxamic acid in lung cancer cells).

Read the full summary ↓

Treatment induced substantial (13%) genomic rearrangement that rebounds despite persistent gene expression changes and spreading of acetylation. The chromatin functional landscape (accessibility, active transcription modification, and gene expression) is controlled and locus-specific, while chromatin contacts are globally altered resulting in a moderate weakening of topologically associating domains. Chromatin states are more dynamic at transcriptionally active loci while genes with reduced expression are epigenetically stable suggesting chromatin architectural turnover and nucleosome remodeling is locus-specific and underlies the bidirectional expression changes. Thus, local 3D chromatin and genome structural dynamics is integral for loci regulation in response to epigenomic perturbation. The partial persistence of these altered features may have larger implications for efficacy of epigenetic drugs in amelioration of disease states.

Published in

Disruption of histone acetylation homeostasis reveals multilayered chromatin regulation for transcriptional resiliency

Venu V, Small EM, Roth C et al. · Epigenetics & chromatin 2025 · PMID 41044756 · doi:10.1186/s13072-025-00631-4

This dataset

Open GSE282758 in finder → Find more human ChIP / ATAC / CUT&Tag datasets →

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 GSE282758_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 PRJNA1135966 and SRA study SRP519925. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41044756) ↗

Study design

3 × 24hr Control ATAC-seq vs 3 × 24hr SAHA Treated ATAC-seq vs 3 × 48hr Control ATAC-seq vs 3 × 48hr SAHA Treated ATAC-seq

Supports a case/control comparison: 6 samples read as cases, 6 as controls.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 of them. 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

GSM8650072 24hr Control ATAC-seq Bio rep 1 24hr Control ATAC-seq
GSM8650073 24hr Control ATAC-seq Bio rep 2 24hr Control ATAC-seq
GSM8650074 24hr Control ATAC-seq Bio rep 3 24hr Control ATAC-seq
GSM8650075 24hr SAHA Treated ATAC-seq Bio rep 1 24hr SAHA Treated ATAC-…
GSM8650076 24hr SAHA Treated ATAC-seq Bio rep 2 24hr SAHA Treated ATAC-…
GSM8650077 24hr SAHA Treated ATAC-seq Bio rep 3 24hr SAHA Treated ATAC-…
GSM8650078 48hr Control ATAC-seq Bio rep 1 48hr Control ATAC-seq
GSM8650079 48hr Control ATAC-seq Bio rep 2 48hr Control ATAC-seq
GSM8650080 48hr Control ATAC-seq Bio rep 3 48hr Control ATAC-seq
GSM8650081 48hr SAHA Treated ATAC-seq Bio rep 1 48hr SAHA Treated ATAC-…
GSM8650082 48hr SAHA Treated ATAC-seq Bio rep 2 48hr SAHA Treated ATAC-…
GSM8650083 48hr SAHA Treated ATAC-seq Bio rep 3 48hr SAHA Treated ATAC-…

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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.