GEO series

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

GSE296241 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2026/05/01 Platform GPL18573Platform GPL19057

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 16 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: 16 samples: 16 samples, each with a distinct title — no replicated groupsGroups 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

Open GSE296241 in finder → Find more ChIP / ATAC / CUT&Tag datasets →

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 GSE296241_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 PRJNA1258262 and SRA study SRP582851. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41949410) ↗

Study design

16 samples, each with a distinct title — no replicated groups

Supports a case/control comparison: 2 samples read as cases, 2 as controls.

How we read this: Read from 16 sample titles: 16 distinct titles with little repetition. 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

GSM8967586 H3K27ac ChIP-seq in DMSO-treated cells, control for 24hr dTAG13 treatment
GSM8967587 H3K27ac ChIP-seq in dTAG13-treated (24hr) SEM cells with MYB endogenously tagged with FKBP12(F36V)
GSM8967588 Input for H3K27ac ChIP-seq in DMSO-treated cells, control for 24hr dTAG13 treatment
GSM8967589 Input for H3K27ac ChIP-seq in dTAG13-treated (24hr) SEM cells with MYB endogenously tagged with FKBP12(F36V)
GSM8967590 FS2 ChIP-seq in E14 (TOT2N variant) cells containing stable integration of TetR constuct
GSM8967591 FS2 ChIP-seq in E14 (TOT2N variant) cells containing stable integration of TetR-MYBTA constuct
GSM8967592 H3K27ac ChIP-seq in E14 (TOT2N variant) cells containing stable integration of TetR constuct
GSM8967593 H3K27ac ChIP-seq in E14 (TOT2N variant) cells containing stable integration of TetR-MYBTA constuct +doxycycline
GSM8967594 H3K27ac ChIP-seq in E14 (TOT2N variant) cells containing stable integration of TetR-MYBTA constuct (control)
GSM8967595 H3K27ac ChIP-seq in E14 (TOT2N variant) cells containing stable integration of TetR-MYBTA constuct
GSM8967596 Input for FS2 ChIP-seq in E14 (TOT2N variant) cells containing stable integration of TetR constuct
GSM8967597 Input for FS2 ChIP-seq in E14 (TOT2N variant) cells containing stable integration of TetR-MYBTA constuct
GSM8967598 Input for H3K27ac ChIP-seq in E14 (TOT2N variant) cells containing stable integration of TetR constuct
GSM8967599 Input for H3K27ac ChIP-seq in E14 (TOT2N variant) cells containing stable integration of TetR-MYBTA constuct
GSM8967600 Input for H3K27ac ChIP-seq in E14 (TOT2N variant) cells with integration of TetR-MYBTA constuct +doxycycline
GSM8967601 Input for H3K27ac ChIP-seq in E14 (TOT2N variant) cells containing stable integration of TetR-MYBTA constuct (control)

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