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The TET protein family interactor PROSER1 sustains hematopoietic stem cell function [ChIP-Seq]

GSE240262 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 15 samples Submitted 2025/06/25 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 15 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
15 samples: 6 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.
Paper
The TET protein family interactor PROSER1 sustains hematopoietic stem cell functionBlood advances · 2025
Summary (written by the submitters)
Ten-Eleven-Translocation (TET) enzymes are epigenetic regulators important for prevention of hematological malignancies. PROSER1, a known TET protein interactor, has a critical role in modulating TET-mediated DNA demethylation during development. However, the potential involvement of PROSER1 in regulation of hematopoiesis and leukemogenesis remains unknown.
Read the full summary ↓
Here, we demonstrate that the leukemia suppressive functions of TET2 are preserved in the absence of PROSER1. Nonetheless, we find that loss of PROSER1 partially recapitulates the aberrant enhancer DNA methylation phenotype observed upon TET2 knockout, suggesting that PROSER1 and TET2 play both cooperative and distinct roles in the regulation of DNA methylation in hematopoiesis. Importantly, using serial hematopoietic stem cell (HSC) transplantation assays, we find progressive exhaustion of HSC activity and reduction in hematopoietic lineage output upon loss of PROSER1. Our findings imply that, beyond the established role of TET2 loss-of-function mutations in promoting HSC expansion and leukemic transformation, accurate TET activity, regulated by PROSER1, is equally important to prevent HSC exhaustion and sustain normal hematopoiesis.
Published in
The TET protein family interactor PROSER1 sustains hematopoietic stem cell function
Knatko EV, Fleming A, Li X et al. · Blood advances 2025 · PMID 40554416 · doi:10.1182/bloodadvances.2024015683
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 GSE240262_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 PRJNA1003062 and SRA study SRP453899. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
wildtype Hoxb8-FL H3K4me1 ChIP biol ×3 Proser1 knockout Hoxb8-FL H3K4me1 biol ×3 wildtype Hoxb8-FL H3K27ac ChIP biol ×2 Proser1 knockout Hoxb8-FL H3K27ac ChIP biol ×2 wildtype Hoxb8-FL H3K27me3 biol ×2 Proser1 knockout Hoxb8-FL H3K27me3 biol ×2 wildtype Hoxb8-FL ChIP input ×1

Supports a case/control comparison: 7 samples read as cases, 8 as controls.

How we read this: 6 replicated groups read from 15 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
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