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ID3 Deficiency Alters Chromatin Accessibility at DSB Sites and Enhances Vulnerability to HDAC Inhibition [ATAC-seq]

GSE301514 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/01/29 Platform GPL21697
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 × ATAC-seq AID-DIvA U2OS control-untreated-biol vs 3 × ATAC-seq AID-DIvA U2OS control-treated-0min-biol vs 3 × ATAC-seq AID-DIvA U2OS knockout-untreated-biol vs 3 × ATAC-seq AID-DIvA U2OS knockout-treated-0min-biolGroups 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
ID3 deficiency alters chromatin accessibility at DSB sites and enhances vulnerability to HDAC inhibitionInternational journal of cancer · 2026
Summary (written by the submitters)
The inhibitor of DNA-binding 3 (ID3) plays a crucial role in DNA double-strand break (DSB) repair. We previously reported that ID3 loss reduced chromatin accessibility at DNA repair gene promoters, yet its exact role in DNA repair via chromatin regulation remained elusive. Using the AID-DIvA cell system with inducible DSBs, we show that ID3 directly regulates chromatin accessibility at DSB sites, as demonstrated by reduced chromatin accessibility and lower H3K27ac levels in ID3-knockout (KO) cells.
Read the full summary ↓
Loss of ID3 renders cells highly sensitive to histone deacetylase (HDAC) inhibition, particularly to the Class I HDAC inhibitor, leading to the accumulation of unrepaired DSBs and delayed cell cycle progression. Transcriptome and proteome analyses revealed that HDAC inhibition in ID3-KO cells results in the downregulation of gene sets involved in the regulation of cell cycle and cell division. The synthetic lethality observed between ID3 loss and Class I HDAC inhibition underscores a novel therapeutic vulnerability in ID3-deficient cancers, driven by compounded defects in chromatin remodeling, cell cycle, and DNA repair. Our study provides new insights into the relationship between chromatin regulation and genome stability, with implications for targeted cancer therapies.
Published in
ID3 deficiency alters chromatin accessibility at DSB sites and enhances vulnerability to HDAC inhibition
Corte GD, Eldesouky H, Puchan J et al. · International journal of cancer 2026 · PMID 41735198 · doi:10.1002/ijc.70400
This dataset
Open GSE301514 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 GSE301514_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 PRJNA1284934 and SRA study SRP596490. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41735198) ↗
Study design
3 × ATAC-seq AID-DIvA U2OS control-untreated-biol vs 3 × ATAC-seq AID-DIvA U2OS control-treated-0min-biol vs 3 × ATAC-seq AID-DIvA U2OS knockout-untreated-biol vs 3 × ATAC-seq AID-DIvA U2OS knockout-treated-0min-biol

Supports a between-group comparison across 12 samples.

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
Datasets on a similar topic

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