GEO series

IRF2BP2 counteracts the ATF7/JDP2 heterodimer to prevent inflammatory overactivation in AML cells [RNA-seq]

GSE229593 Homo sapiens (human) RNA-seq (gene expression) 21 samples Submitted 2024/05/07 Platform GPL24676

At a glance

RNA-seq (gene expression) · human · 21 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Homo sapiens (human)
Topic: Acute myeloid leukemiaThis series is part of our curated briefing on it.
Samples: 21 samples: 8 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.
Paper: IRF2BP2 counteracts the ATF7/JDP2 AP-1 heterodimer to prevent inflammatory overactivation in acute myeloid leukemia (AML) cellsNucleic acids research · 2024

Summary (written by the submitters)

Acute myeloid leukemia (AML) is a hematological malignancy characterized by abnormal proliferation and accumulation of immature myeloid cells in the bone marrow. Inflammation plays a crucial role in AML progression, but excessive activation of cell-intrinsic inflammatory pathways can also trigger cell death. IRF2BP2 is a chromatin regulator implicated in AML pathogenesis, although its precise role in this disease is not fully understood.

Read the full summary ↓

In this study, we demonstrate that IRF2BP2 interacts with the AP-1 heterodimer ATF7/JDP2, which is involved in activating inflammatory pathways in AML cells. We show that IRF2BP2 is recruited by the ATF7/JDP2 dimer to chromatin and counteracts its gene-activating function. Loss of IRF2BP2 leads to overactivation of inflammatory pathways, resulting in strongly reduced proliferation. Our research indicates that a precise equilibrium between activating and repressive transcriptional mechanisms creates a pro-oncogenic inflammatory environment in AML cells. The ATF7/JDP2-IRF2BP2 regulatory axis is likely a key regulator of this process and may, therefore, represent a promising therapeutic vulnerability for AML. Thus, our study provides new insights into the molecular mechanisms underlying AML pathogenesis and identifies a potential therapeutic target for AML treatment.

Published in

IRF2BP2 counteracts the ATF7/JDP2 AP-1 heterodimer to prevent inflammatory overactivation in acute myeloid leukemia (AML) cells

Fischer S, Weber LM, Stielow B et al. · Nucleic acids research 2024 · PMID 38801077 · doi:10.1093/nar/gkae437

This dataset

Open GSE229593 in finder → Find more human RNA-seq datasets → Acute myeloid leukemia landscape →

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 GSE229593_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA955111 and SRA study SRP432416. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 38801077) ↗

Study design

8 conditions, mostly in duplicate

RNA-Seq shRNA1 IRF2BP2 ×3 RNA-Seq shRNA2 IRF2BP2 ×3 RNA-Seq shRNA Control ×2 RNA-Seq KO Control ×2 RNA-Seq KO1 ATF7 ×2 RNA-Seq KO2 ATF7 ×2 RNA-Seq KO1 JDP2 ×2 RNA-Seq KO2 JDP2 ×2 +3 more

Supports a between-group comparison across 18 samples.

How we read this: 8 replicated groups read from 21 sample titles; they account for 18 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

GSM7165906 RNA-Seq shRNA Control repl1 RNA-Seq shRNA Control
GSM7165907 RNA-Seq shRNA Control repl2 (low quality)
GSM7165908 RNA-Seq shRNA Control repl3 RNA-Seq shRNA Control
GSM7165909 RNA-Seq shRNA1 IRF2BP2 repl1 RNA-Seq shRNA1 IRF2BP2
GSM7165910 RNA-Seq shRNA1 IRF2BP2 repl2 RNA-Seq shRNA1 IRF2BP2
GSM7165911 RNA-Seq shRNA1 IRF2BP2 repl3 RNA-Seq shRNA1 IRF2BP2
GSM7165912 RNA-Seq shRNA2 IRF2BP2 repl1 RNA-Seq shRNA2 IRF2BP2
GSM7165913 RNA-Seq shRNA2 IRF2BP2 repl2 RNA-Seq shRNA2 IRF2BP2
GSM7165914 RNA-Seq shRNA2 IRF2BP2 repl3 RNA-Seq shRNA2 IRF2BP2
GSM7165915 RNA-Seq WT repl1 (low quality)
GSM7165916 RNA-Seq WT repl2
GSM7165917 RNA-Seq KO Control repl1 RNA-Seq KO Control
GSM7165918 RNA-Seq KO Control repl2 RNA-Seq KO Control
GSM7165919 RNA-Seq KO1 ATF7 repl1 RNA-Seq KO1 ATF7
GSM7165920 RNA-Seq KO1 ATF7 repl2 RNA-Seq KO1 ATF7
GSM7165921 RNA-Seq KO2 ATF7 repl1 RNA-Seq KO2 ATF7
GSM7165922 RNA-Seq KO2 ATF7 repl2 RNA-Seq KO2 ATF7
GSM7165923 RNA-Seq KO1 JDP2 repl1 RNA-Seq KO1 JDP2
GSM7165924 RNA-Seq KO1 JDP2 repl2 RNA-Seq KO1 JDP2
GSM7165925 RNA-Seq KO2 JDP2 repl1 RNA-Seq KO2 JDP2
GSM7165926 RNA-Seq KO2 JDP2 repl2 RNA-Seq KO2 JDP2

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GSE229594 IRF2BP2 counteracts the ATF7/JDP2 heterodimer to prevent inflammatory overactivation in AML cells [ChIP-seq] 15 samples shares irf2bp2, atf7, jdp2, aml, overactivation, counteracts, heterodimer, prevent
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