← BioTransfer GEO Dataset Finder
GEO series

H3K79me2 Profiling Reveals DOT1L Regulated Splicing in MLL-rearranged AML [ChIP-Seq]

GSE320036 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 56 samples Submitted 2026/02/26 Platform GPL21290
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 56 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
56 samples
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)
Aberrant H3K79 dimethylation by DOT1L is a defining feature of MLL-rearranged (MLLr) acute myeloid leukemia (AML), but whether this modification influences alternative splicing remains unclear. Here, we performed H3K79me2 ChIP-seq and RNA-seq on primary samples from 24 MLLr AML patients, 4 wild-type MLL AML patients, and 4 healthy bone marrow donors.
Read the full summary ↓
We found that a subset of exon skipping (SE) events was enriched at H3K79me2-occupied loci in MLLr samples. DOT1L inhibition with EPZ5676 led to broad changes in SE patterns, and many switched events showed concurrent reduction in local H3K79me2 signal. Pathway analysis of genes harboring these events revealed enrichment for RNA processing and splicing-related functions, with additional involvement of DNA repair and apoptosis-associated pathways. To identify potential mediators, we performed rapid immunoprecipitation mass spectrometry (RIME) in MV4-11 and MOLM-14 cells and detected SRSF2 and hnRNP family proteins in complex with DOT1L; these interactions were confirmed by co-immunoprecipitation. Combined inhibition of DOT1L and selected splicing factors reduced cell proliferation more effectively than single-agent treatment, both in MLLr cell lines and in xenograft models. These results indicate that H3K79me2 contributes to alternative splicing regulation through splicing factor recruitment in MLLr AML and provide a rationale for coordinated epigenetic–splicing therapeutic strategies.
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 GSE320036_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 PRJNA1426031 and SRA study SRP678294. Searching any of these in the dataset finder brings you back here.

Samples in this study

The sample list for this study is not cached yet. Press Load samples and it will be fetched from NCBI.

+ 56 more — browse all 56 samples with per-sample file links →

More Acute myeloid leukemia datasets

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

Share this dataset

Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.