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Dissecting FOXA1 pioneering function by acute pharmacological degradation.

GSE315959 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 51 samples Submitted 2026/02/25 Platform GPL34295Platform GPL30173
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 51 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
51 samples: 16 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.
Summary (written by the submitters)
Pioneer factors control transcription by opening chromatin, but a lack of chemical tools has made it difficult to study pioneer activity with kinetic precision. We recently reported covalent chemical probes that remodel the genomic localization of FOXA1, a prototypical pioneer factor essential for the growth of many breast and prostate cancers.
Read the full summary ↓
Here, we expand the chemical toolbox for FOXA1 by developing a dTAG-based system for small molecule-induced FOXA1 degradation. Coupling pharmacological perturbations to rapid measurements of chromatin structure and function, we find that FOXA1 exclusively initiates chromatin opening at its genomic binding sites, but, interestingly, this unidirectional outcome both activates and represses gene transcription depending on the chromatin environment surrounding FOXA1-binding sites. These effects apply to both androgen receptor (AR) target genes and other FOXA1 targets. Our findings thus uncover regulatory features that translate FOXA1 pioneering activity into both activation and repression of transcriptional programs critical for cancer growth.
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 GSE315959_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 PRJNA1400010 and SRA study SRP660701. Searching any of these in the dataset finder brings you back here.

Study design
16 conditions, mostly in triplicate
22Rv1-dTAG-FOXA1, DMSO, 3h, biol ×3 22Rv1-dTAG-FOXA1, DMSO, 8h, biol ×3 22Rv1-dTAG-FOXA1, dTAGv1, 8h, biol ×3 22Rv1-dTAG-FOXA1, DMSO, 24h, biol ×3 22Rv1-dTAG-FOXA1, dTAGv1, 24h, biol ×3 22Rv1-dTAG-FOXA1, DMSO, 8h, BMSstudy, biol ×3 22Rv1-dTAG-FOXA1, BMS-986365, 8h, biol ×3 22Rv1-dTAG-FOXA1, DMSO, 24h, BMSstudy, biol ×3 +13 more

Supports a between-group comparison across 46 samples.

How we read this: 16 replicated groups read from 51 sample titles; they account for 46 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

+ 11 more — browse all 51 samples with per-sample file links →

Datasets on a similar topic

Search all human ChIP / ATAC / CUT&Tag datasets in GEO →

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