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Chromatin accessibility profiling of IMR-90 SV40-T cells expressing wild-type and mutant H2B

GSE307869 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/03/02 Platform GPL24676
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: 6 conditions, mostly in duplicateGroups 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
Nucleosome stability safeguards cell identity, stress resilience and healthy agingResearch square · 2025
Summary (written by the submitters)
Nucleosomes are the minimal repeating units of chromatin. Their dynamic assembly and disassembly underpins chromatin organization and genome regulation. However, how intrinsic nucleosome stability contributes to higher-level yet fundamental cellular and organismal properties—such as preservation of cell identity, lineage specification, stress resilience and healthy aging—remains unclear.
Read the full summary ↓
To address this, we tested the impact of intrinsic nucleosome instability across multiple cell, tissue and organismal models by introducing histone mutants that weaken histone–histone interactions. Despite no overt effects on global chromatin accessibility, DNA damage, steady-state proliferation or cell viability, nucleosome instability impaired lineage-specific gene expression programs, altered lineage specification and activated intrinsic inflammatory and stress pathways in a manner reminiscent of aging in mouse tissues and human cells. Consistently, in Caenorhabditis elegans and Drosophila melanogaster, nucleosome instability accelerated the onset of age-associated transcriptional alterations and functional decline in Caenorhabditis elegans and Drosophila melanogaster, and . At the cellular level, nucleosome instability also heightened cellular sensitivity vulnerability to exogenous perturbations—including environmental, epigenetic and mitotic stress—in human cells and Saccharomyces cerevisiaeyeast. These cross-species findings identify nucleosome stability as an evolutionarily conserved epigenetic safeguard that preserves cell identity and stress resilience, sustaining organismal function and longevity.
Published in
Nucleosome stability safeguards cell identity, stress resilience and healthy aging
Adams P, Tanaka H, McCauley B et al. · Research square 2025 · PMID 41333395 · doi:10.21203/rs.3.rs-7913970/v1
This dataset
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.

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 GSE307869_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1327445 and SRA study SRP619333. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
ATAC-Seq, IMR-90 SV40-T cells, Empty, ×2 ATAC-Seq, IMR-90 SV40-T cells, WT, ×2 ATAC-Seq, IMR-90 SV40-T cells, E76K, ×2 ATAC-Seq, IMR-90 SV40-T cells, Empty, TGFβ1, ×2 ATAC-Seq, IMR-90 SV40-T cells, WT, TGFβ1, ×2 ATAC-Seq, IMR-90 SV40-T cells, E76K, TGFβ1, ×2

Supports a between-group comparison across 12 samples.

How we read this: 6 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
Datasets on a similar topic

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