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A pathogenic GATA2 zinc finger mutation restricts chromatin occupancy in human erythroid progenitor cells

GSE288701 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 36 samples Submitted 2025/12/03 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 36 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
36 samples: 10 conditions, mostly with about 4 replicates eachGroups 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
GATA2 decommissioning of enhancers: A mechanism to constrain inflammatory signalingCell reports · 2025
Summary (written by the submitters)
The transcription factor GATA2 regulates hematopoietic stem and progenitor production and function via interactions with other regulatory proteins at gene enhancers and promoters. Genome-wide patterns of GATA2 chromatin occupancy differ by cell type; dynamically controlled by levels of GATA2 and associated proteins. During erythroid differentiation, gene expression networks that drive the process are established upon displacement of GATA2 from regulatory elements by the related transcription factor GATA1.
Read the full summary ↓
Herein, we map sites of GATA2 chromatin occupancy in the human erythroid progenitor cell line HUDEP-2 and define the genes regulated by GATA2 in these cells. Additionally, we show that a human pathogenic GATA2 mutation, T354M, restricts GATA2 occupancy to a subset of chromatin sites.
Published in
GATA2 decommissioning of enhancers: A mechanism to constrain inflammatory signaling
Jung MM, Tran VL, Xiong Y et al. · Cell reports 2025 · PMID 41004342 · doi:10.1016/j.celrep.2025.116344
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 GSE288701_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 PRJNA1219096 and SRA study SRP561457. Searching any of these in the dataset finder brings you back here.

Study design
10 conditions, mostly with about 4 replicates each
GATA2 low HUDEP-2, lentiviral HA-GATA2(T354M)… ×4 GATA2 low HUDEP-2, lentiviral HA-GATA2, IgG i… ×4 GATA2 low HUDEP-2, lentiviral HA-GATA2, HA an… ×4 GATA2 low HUDEP-2, lentiviral empty vector, H… ×4 GATA2 low HUDEP-2, lentiviral HA-GATA2(T354M)… ×4 GATA2 low HUDEP-2, lentiviral HA-GATA2, GATA2… ×4 GATA2 low HUDEP-2, lentiviral empty vector, G… ×4 HUDEP-2, lentiviral empty vector, GATA2 antib… ×4 +2 more

Supports a between-group comparison across 36 samples.

How we read this: 10 replicated groups read from 36 sample titles; they account for 36 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
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