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Pivotal Role of the NuRD Complex in Remodeling Chromatin Environment and Maintaining Genome Architecture at CTCF Sites [hESC_H9_d049_ChIP_Seq]

GSE215328 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 135 samples Submitted 2026/05/04 Platform GPL23227
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 135 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
135 samples: 13 conditions, mostly in triplicateGroups 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
NuRD-enabled CTCF-TET crosstalk orchestrates epigenome reprogramming and genome architectureMolecular cell · 2026
Summary (written by the submitters)
CCCTC-binding factor (CTCF) is an evolutionarily conserved transcription factor with diverse regulatory roles. Around stable CTCF binding sites, nucleosomes are highly ordered and DNA methylation is reduced, yet the mechanisms establishing and maintaining this epigenetic environment remain unclear. Utilizing an innovative eBioID method, we identified that virtually all subunits of the nucleosome remodeling and deacetylase (NuRD) complex are associated with CTCF in cells.
Read the full summary ↓
Further analyses revealed that the NuRD complex is necessary for the chromatin binding of CTCF, and emerges as a novel regulator of the genome architecture. Additionally, we discovered that MBD3-NuRD facilitates the recruitment of TET demethylases to CTCF sites, initiating local DNA demethylation essential for the activation of adjacent gene expression. Embryonic stem cells deficient in the NuRD complex showed impaired lineage commitment. In summary, this study elucidates a mechanism illustrating the interplay between CTCF binding and the epigenome including 3D genome organization and DNA methylation, with the NuRD complex serving as an indispensable mediator.
Published in
NuRD-enabled CTCF-TET crosstalk orchestrates epigenome reprogramming and genome architecture
Sun W, Wu N, Xia M et al. · Molecular cell 2026 · PMID 42225060 · doi:10.1016/j.molcel.2026.05.010
This dataset
Open GSE215328 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 GSE215328_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 PRJNA889778 and SRA study SRP402202. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42225060) ↗
Study design
13 conditions, mostly in triplicate
hESC_H9_d0_WT_input ×3 hESC_H9_d0_WT_IP_CTCF ×3 hESC_H9_d0_WT_IP_MBD3 ×3 hESC_H9_d4_WT_input ×3 hESC_H9_d4_WT_IP_CTCF ×3 hESC_H9_d4_WT_IP_MBD3 ×3 hESC_H9_d9_WT_input ×3 hESC_H9_d9_WT_IP_CTCF ×3 +6 more

Supports a between-group comparison across 39 samples.

How we read this: 13 replicated groups read from the first 40 of 135 sample titles; they account for 39 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

+ 95 more — browse all 135 samples with per-sample file links →

Datasets on a similar topic

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