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Sustained MYB activity drives emergent enhancer activation and precise enhancer-promoter interactions [ATAC-seq]

GSE296152 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 9 samples Submitted 2026/05/01 Platform GPL19057
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 9 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
Mus musculus (mouse)
Samples
9 samples: 3 × ATAC-seq in E14 (TOT2N variant) cells containing stable integration of TetR constuct, vs 3 × ATAC-seq in E14 (TOT2N variant) cells containing stable integration of TetR-MYBTA constuct, vs 3 × ATAC-seq in wild type E14 (TOT2N variant) cells,Groups 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
MYB activity drives emergent enhancer activation and enhancer-promoter interactions in acute lymphoblastic leukemiaBlood · 2026
Summary (written by the submitters)
Transcription factors (TFs) are key effectors of enhancer activity. MYB is a critical hematopoietic TF that is frequently dysregulated in cancer. Despite its well-established role, the exact mechanisms by which MYB influences enhancer function—and the specific stages of enhancer activation at which it operates—remain poorly understood.
Read the full summary ↓
Using high resolution Micro-Capture-C, we show that upon MYB degradation, highly defined enhancer-promoter interactions at specific MYB binding sites are lost. Loss of these interactions, together with other hallmarks of enhancer activity—reduced H3 lysine-27 acetylation and enhancer RNA transcription—correlates with significant downregulation of target gene expression in leukemia, indicating that MYB mediates transcription activation via maintenance of enhancer function. When anchored to DNA within a gene desert region that is devoid of histone marks and active transcription, the MYB transactivation domain is sufficient and necessary for the nucleation of an enhancer-like region. This results in the activation of transcription from distal cryptic elements and the establishment of long-range chromatin interactions up to 400 kb away from the anchor point. Together, these results indicate that MYB activity alone is sufficient to induce long-range interactions and transcription, achieving this through highly precise enhancer-promoter crosstalk.
Published in
MYB activity drives emergent enhancer activation and enhancer-promoter interactions in acute lymphoblastic leukemia
Lau IJ, Bloye G, Smith AL et al. · Blood 2026 · PMID 41949410 · doi:10.1182/blood.2025030424
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 GSE296152_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 PRJNA1257929 and SRA study SRP582695. Searching any of these in the dataset finder brings you back here.

Study design
3 × ATAC-seq in E14 (TOT2N variant) cells containing stable integration of TetR constuct, vs 3 × ATAC-seq in E14 (TOT2N variant) cells containing stable integration of TetR-MYBTA constuct, vs 3 × ATAC-seq in wild type E14 (TOT2N variant) cells,

Supports a between-group comparison across 9 samples.

How we read this: 3 replicated groups read from 9 sample titles; they account for 9 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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