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SUV39H1/2-mediated H3K9me3 restricts TE-induced immune response in Acute Myeloid Leukemia [ChIP-Seq]

GSE285122 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 18 samples Submitted 2026/06/17 Platform GPL34284
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 18 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)
Topic
Acute myeloid leukemiaThis series is part of our curated briefing on it.
Samples
18 samples: 7 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)
Histone 3 Lysine 9 tri-methylation (H3K9me3) is a heterochromatin-associated histone mark deposited broadly across the genome and its regulation is required in normal hematopoiesis. Furthermore, H3K9me3 has been linked with 3D genome organization. However, in the context of acute myeloid leukemia (AML), the regulation of H3K9me3 and its function in 3D genome architecture remained understudied.
Read the full summary ↓
In this study, through systematic Knockdowns and Knockouts, we identified SUV39H1 and by part its paralogue SUV39H2 as the major H3K9me3 depositors in AML. We demonstrated the role of SUV39H1/2 in establishing global H3K9me3 levels in AML cells and showed H3K9me3 depletion upon SUV39H1/2 Knockout preferentially occurred at sub-megabase level broad peaks and in GC poor regions. Loss of SUV39H1/2-mediated H3K9me3 poised AML cells towards monocyte/macrophage differentiation, induced TE re-activation and interferon response activation, and reduced AML cell growth and clonogenicity in vitro. Analysis of higher-order chromatin architecture reveals that while SUV39H1/2-mediated H3K9me3 is associated with a small fraction of larger chromatin structures, loss of SUV39H1/2 drives concomitant increase of H3K27me3 at B compartments. Taken together, our findings characterize the regulation of SUV39H1/2-mediated H3K9me3 and reveal its role in leukemogenesis and higher-order chromatin structure.
This dataset
Open GSE285122 in finder → Find more human ChIP / ATAC / CUT&Tag 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 GSE285122_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1201210 and SRA study SRP553041. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
7 conditions, mostly in duplicate
U937 sgControl Cells H3K9me3 ChIP, ×2 U937 SKO Cells H3K9me3 ChIP, ×2 U937 DKO Cells H3K9me3 ChIP, ×2 U937 sgControl Cells H3K27me3 ChIP, ×2 U937 SKO Cells H3K27me3 ChIP, ×2 U937 DKO Cells H3K27me3 ChIP, ×2 U937 WT Cells SETDB1 ChIP, ×2 U937 sgControl Cells Input ×1 +3 more

Supports a between-group comparison across 14 samples.

How we read this: 7 replicated groups read from 18 sample titles; they account for 14 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
More Acute myeloid leukemia datasets

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