GEO series

SWI/SNF complex-mediated ZNF410 cooperative binding maintains chromatin accessibility and enhancer activity [ChIP-Seq]

GSE256316 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 121 samples Submitted 2025/03/22 Platform GPL24676

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 121 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: 121 samples: 121 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.
Paper: SWI/SNF complex-mediated ZNF410 cooperative binding maintains chromatin accessibility and enhancer activityCell reports · 2025

Summary (written by the submitters)

Clustering of multiple transcription factor binding sites (TFBSs) for the same TF has proved to be a pervasive feature of cis-regulatory elements in eukaryotic genome. However, contribution of binding sites within the homotypic clusters of TFBSs (HCTs) to TF binding and target gene expression remains to be understood. Here, we characterize the CHD4 enhancers that harbor unique functional ZNF410 HCTs genome-wide.

Read the full summary ↓

We uncover that ZNF410 controls chromatin accessibility and activity of the CHD4 enhancer regions. We demonstrate that ZNF410 binds to the HCTs in a collaborative fashion, further conferring transcriptional activation. Especially, three ZNF410 motifs (sub-HCTs) located at 3´ end of the distal enhancer act as “switch motifs” to control the chromatin accessibility and enhancer activity. Mechanistically, SWI/SNF complex is selectively required to mediate cooperative ZNF410 binding for CHD4 expression. Together, our findings expose a complex functional hierarchy of homotypic clustered motifs, which cooperates to fine-tune target gene expression.

Published in

SWI/SNF complex-mediated ZNF410 cooperative binding maintains chromatin accessibility and enhancer activity

Xu S, Peng C, Ren R et al. · Cell reports 2025 · PMID 40158221 · doi:10.1016/j.celrep.2025.115476

This dataset

Open GSE256316 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 GSE256316_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 PRJNA1079002 and SRA study SRP490909. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40158221) ↗

Study design

121 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 121 sample titles: 121 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

GSM8093602 K562, input, ChIP-seq
GSM8093603 K562, anti-ZNF410, ZNF410-sgNeg2, rep1, ChIP-seq
GSM8093604 K562, anti-ZNF410, ZNF410-sgNeg2, rep2, ChIP-seq
GSM8093605 K562, anti-ZNF410, ZNF410-sgRNA, rep1, ChIP-seq
GSM8093606 K562, anti-ZNF410, ZNF410-sgRNA, rep2, ChIP-seq
GSM8093607 K562, anti-H3K27ac, ZNF410-sgNeg2, rep1, ChIP-seq
GSM8093608 K562, anti-H3K27ac, ZNF410-sgNeg2, rep2, ChIP-seq
GSM8093609 K562, anti-H3K27ac, ZNF410-sgRNA, rep1, ChIP-seq
GSM8093610 K562, anti-H3K27ac, ZNF410-sgRNA, rep2, ChIP-seq
GSM8093611 K562, anti-H3K4me3, ZNF410-sgNeg2, rep1, ChIP-seq
GSM8093612 K562, anti-H3K4me3, ZNF410-sgNeg2, rep2, ChIP-seq
GSM8093613 K562, anti-H3K4me3, ZNF410-sgRNA, rep1, ChIP-seq
GSM8093614 K562, anti-H3K4me3, ZNF410-sgRNA, rep2, ChIP-seq
GSM8093615 K562, anti-ZNF410, dCas9-KRAB-sgNeg2, rep1, ChIP-seq
GSM8093616 K562, anti-ZNF410, dCas9-KRAB-sgNeg2, rep2, ChIP-seq
GSM8093617 K562, anti-ZNF410, dCas9-KRAB-sgRNA_AL, rep1, ChIP-seq
GSM8093618 K562, anti-ZNF410, dCas9-KRAB-sgRNA_AL, rep2, ChIP-seq
GSM8093619 K562, anti-ZNF410, dCas9-KRAB-sgRNA_BK, rep1, ChIP-seq
GSM8093620 K562, anti-ZNF410, dCas9-KRAB-sgRNA_BK, rep2, ChIP-seq
GSM8093621 K562, anti-H3K27ac, dCas9-KRAB-sgNeg2, rep1, ChIP-seq
GSM8093622 K562, anti-H3K27ac, dCas9-KRAB-sgNeg2, rep2, ChIP-seq
GSM8093623 K562, anti-H3K27ac, dCas9-KRAB-sgRNA_AL, rep1, ChIP-seq
GSM8093624 K562, anti-H3K27ac, dCas9-KRAB-sgRNA_AL, rep2, ChIP-seq
GSM8093625 K562, anti-H3K27ac, dCas9-KRAB-sgRNA_BK, rep1, ChIP-seq
GSM8093626 K562, anti-H3K27ac, dCas9-KRAB-sgRNA_BK, rep2, ChIP-seq
GSM8093627 K562, anti-H3K9me3, dCas9-KRAB-sgNeg2, rep1, ChIP-seq
GSM8093628 K562, anti-H3K9me3, dCas9-KRAB-sgNeg2, rep2, ChIP-seq
GSM8093629 K562, anti-H3K9me3, dCas9-KRAB-sgRNA_AL, rep1, ChIP-seq
GSM8093630 K562, anti-H3K9me3, dCas9-KRAB-sgRNA_AL, rep2, ChIP-seq
GSM8093631 K562, anti-H3K9me3, dCas9-KRAB-sgRNA_BK, rep1, ChIP-seq
GSM8093632 K562, anti-H3K9me3, dCas9-KRAB-sgRNA_BK, rep2, ChIP-seq
GSM8093633 K562, anti-H3K4me3, dCas9-KRAB-sgNeg2, rep1, ChIP-seq
GSM8093634 K562, anti-H3K4me3, dCas9-KRAB-sgNeg2, rep2, ChIP-seq
GSM8093635 K562, anti-H3K4me3, dCas9-KRAB-sgRNA_AL, rep1, ChIP-seq
GSM8093636 K562, anti-H3K4me3, dCas9-KRAB-sgRNA_AL, rep2, ChIP-seq
GSM8093637 K562, anti-H3K4me3, dCas9-KRAB-sgRNA_BK, rep1, ChIP-seq
GSM8093638 K562, anti-H3K4me3, dCas9-KRAB-sgRNA_BK, rep2, ChIP-seq
GSM8093639 K562, anti-ZNF410, MT_WT_clone, rep1, ChIP-seq
GSM8093640 K562, anti-ZNF410, MT_WT_clone, rep2, ChIP-seq
GSM8093641 K562, anti-ZNF410, MT1_clone, rep1, ChIP-seq

+ 81 more — browse all 121 samples with per-sample file links →

Datasets on a similar topic

GSE256317 SWI/SNF complex-mediated ZNF410 cooperative binding maintains chromatin accessibility and enhancer activity [ATAC-Seq] 32 samples shares znf410, swi, snf, complex-mediated, accessibility, cooperative, maintains, chromatin
GSE261988 SWI/SNF is a gatekeeper of chromatin access at enhancer networks controlling triple-negative breast cancer progression [ChIP-Seq] 79 samples shares swi, snf, chromatin
GSE328419 CBFA2T3-GLIS2 fusion-mediated mSWI/SNF chromatin remodeler disruption generates cancer-specific dependencies in AMKL [Cut & Run M-07e] 34 samples shares swi, snf, chromatin
GSE294015 Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation (human cell) 32 samples shares swi, snf, chromatin
GSE328418 CBFA2T3-GLIS2 fusion-mediated mSWI/SNF chromatin remodeler disruption generates cancer-specific dependencies in AMKL [Cut&Tag WSU-AML] 25 samples shares swi, snf, chromatin
GSE328420 CBFA2T3-GLIS2 fusion-mediated mSWI/SNF chromatin remodeler disruption generates cancer-specific dependencies in AMKL [Cut & Tag cell lines] 24 samples shares swi, snf, chromatin
GSE328416 CBFA2T3-GLIS2 fusion-mediated mSWI/SNF chromatin remodeler disruption generates cancer-specific dependencies in AMKL [Cut & Run] 19 samples shares swi, snf, chromatin
GSE262093 SWI/SNF Chromatin Remodeling Complex Orchestrates Sequential Binding of Key Transcription Factors in B Cells and Restricts Aggressive Lymphoma [human ChIP-seq] 14 samples shares swi, snf, chromatin

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