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CBFβ-SMMHC-driven leukemogenesis requires enhanced RUNX1-DNA binding affinity in mice

GSE285824 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 38 samples Submitted 2025/06/23 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 38 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
38 samples: 8 conditions, mostly in triplicateGroups 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
CBFβ-SMMHC-driven leukemogenesis requires enhanced RUNX1-DNA binding affinity in miceThe Journal of clinical investigation · 2025
Summary (written by the submitters)
The leukemia fusion gene CBFB-MYH11 requires RUNX1 for leukemogenesis, but the underlying mechanism is unclear. By in vitro studies, we found that CBFβ-SMMHC, the chimeric protein encoded by CBFB-MYH11, could enhance the binding affinity between RUNX1 and its target DNA. Increased RUNX1-DNA binding was also observed in myeloid progenitor cells from mice expressing CBFβ-SMMHC.
Read the full summary ↓
Moreover, only CBFβ-SMMHC variants able to enhance the DNA binding affinity by RUNX1 could induce leukemia in mouse models. Significant transcriptomic changes, affecting genes associated with inflammatory response and target genes of CBFA2T3, were observed in mice expressing leukemogenic CBFβ-SMMHC variants. Finally, we show that CBFβ-SMMHC could not induce leukemia in mice with a Runx1-R188Q mutation, which reduces RUNX1 DNA binding but not affecting its interaction with CBFβ-SMMHC or its sequestration to cytoplasm by CBFβ-SMMHC. Our data suggest that enhancing RUNX1-target DNA binding affinity is an important mechanism of leukemogenesis by CBFβ-SMMHC.
Published in
CBFβ-SMMHC-driven leukemogenesis requires enhanced RUNX1-DNA binding affinity in mice
Zhen T, Cao Y, Dou T et al. · The Journal of clinical investigation 2025 · PMID 40763310 · doi:10.1172/JCI192923
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 GSE285824_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 PRJNA1206157 and SRA study SRP555160. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly in triplicate
RNA-seq_control ×3 RNA-seq_Cbfb-MYH11-mDE ×3 RNA-seq_Cbfb-MYH11-dHABD ×3 RNA-seq_Cbfb-MYH11-KI ×3 RNA-seq_Mx1CreKI ×3 RNA-seq_R188QCreKI ×3 10x-scRNA-seq_Mx1CreKI ×2 10x-scRNA-seq_R188QCreKI ×2 +16 more

Supports a between-group comparison across 22 samples.

How we read this: 8 replicated groups read from 38 sample titles; they account for 22 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
Datasets on a similar topic

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