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Dynamicity of Topoisomerase 1 binding at super-enhancers regulates TLR-responsive gene expression program in macrophages

GSE333477 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 106 samples Submitted 2026/05/28 Platform GPL17021Platform GPL24676Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 106 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
Mus musculus (mouse)
Samples
106 samples: 38 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.
Summary (written by the submitters)
Toll-like receptor (TLR) activation elicits an effective innate immune response by inducing the expression of primary and secondary response genes (PRGs and SRGs). Topoisomerase 1 (TOP1) has emerged as a critical regulator of innate immune responses; however, its mechanism of action remains largely unclear. Here, we demonstrate that ectopic expression of TOP1 is sufficient to program TLR-response in naïve macrophages and its catalytic activity is essential for inducible gene expression.
Read the full summary ↓
TOP1 preferentially localizes to super-enhancers and TLR activation results in rapid redistribution of TOP1 from resting-state super-enhancers to stimulus-gained super-enhancers, leading to a transcriptional switch. Notably, TOP1 facilitates the recruitment of BRG1 to stimulus-gained super-enhancers. The cooperation between TOP1 and BRG1 enhances the chromatin accessibility at super-enhancers to preferentially regulate the expression of SRGs. These findings establish TOP1 as an epigenomic regulator that links chromatin remodeling at active super-enhancers with inducible gene expression in response to pathogenic stimuli.
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 GSE333477_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 PRJNA1471146 and SRA study SRP704169. Searching any of these in the dataset finder brings you back here.

Study design
38 conditions, mostly in duplicate
Con_WT_BMDM ×6 LPS_WT_BMDM ×4 Topo_LPS_WT_BMDM ×4 ChIP_RNAPolII_Con_WT_BMDM ×3 Con_FL_BMDM ×2 Pam3CSK4_FL_BMDM ×2 FSL_FL_BMDM ×2 Imiquimod_FL_BMDM ×2 +51 more

Supports a between-group comparison across 85 samples.

How we read this: 38 replicated groups read from 106 sample titles; they account for 85 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

+ 66 more — browse all 106 samples with per-sample file links →

Datasets on a similar topic

Search all 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.