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Mutant CEBPA promotes tolerance to inflammatory stress through deficient AP-1 activation [ChIP-seq]

GSE270547 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 40 samples Submitted 2025/03/11 Platform GPL34290Platform GPL34284Platform GPL28457
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 40 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
40 samples: 10 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)
The CEBPA transcription factor is frequently mutated in acute myeloid leukemia (AML). Mutations in the CEBPA gene, which are typically biallelic, result in the production of a shorter isoform known as p30. Both the canonical 42-kDa isoform (p42) and the AML-associated p30 isoform bind chromatin and activate transcription, but the specific transcriptional programs controlled by each protein and how they are linked to a selective advantage in AML is not well understood.
Read the full summary ↓
Here, we show that cells expressing the AML-associated p30 have reduced baseline inflammatory gene expression and display altered dynamics of transcriptional induction in response to LPS, consequently impacting cytokine secretion. This confers p30-expressing cells an increased resistance to the adverse effects of prolonged exposure to inflammatory signals. Mechanistically, we show that these differences primarily result from the differential regulation of AP-1 family proteins. In addition, we find that the altered function of the AP-1 member ATF4 in p30-expressing cells alters their response to ER stress. Collectively, these findings uncover a novel link between mutant CEBPA, inflammation and the stress response, potentially revealing a new vulnerability in AML.
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 GSE270547_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 PRJNA1127477 and SRA study SRP516153. Searching any of these in the dataset finder brings you back here.

Study design
10 conditions, mostly in triplicate
HPC-7, p30, LPS 2h, H3K27Ac, ChIP, ×3 HPC-7, p30, UT, H3K27Ac, ChIP, ×3 HPC-7, p42, LPS 2h, H3K27Ac, ChIP, ×3 HPC-7, p42, UT, H3K27Ac, ChIP, ×3 HPC-7, p30, LPS 2h, INPUT, ×3 HPC-7, p30, UT, INPUT, ×3 HPC-7, p42, LPS 2h, INPUT, ×3 HPC-7, p42, UT, INPUT, ×3 +14 more

Supports a between-group comparison across 28 samples.

How we read this: 10 replicated groups read from 40 sample titles; they account for 28 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
Datasets on a similar topic

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