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Methylation of SRSF2P95H by SETD2 suppresses myeloid-derived suppressor cell function by inhibiting inflammatory signaling in myelodysplastic syndrome

GSE265871 Mus musculus (mouse) DNA methylation 13 samples Submitted 2025/10/24 Platform GPL24247
At a glance

DNA methylation · mouse · 13 samples

What it is
DNA methylationChemical marks on DNA that help switch genes on or off.
Organism
Mus musculus (mouse)
Samples
13 samples: 13 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.
Summary (written by the submitters)
Myelodysplastic syndrome (MDS) is a malignant hematologic cancer accompanied with ineffective hematopoietic and myeloid bias. MDS patients with the SRSF2 mutation have a poor prognosis and require specific and effective therapeutic agents. Here, we find that the low expression of SETD2 in the SRSF2P95H background is associated with anomalously increased myeloid derived suppressor cells (MDSCs) differentiation and inflammatory response.
Read the full summary ↓
Our results reveal that the low expression of SETD2 in the hematopoietic stem and progenitor cells (HSPCs) of MDS patients with SRSF2P95H/+ is associated with patient outcomes. The deletion of Setd2 in Srsf2P95H/+ mice led to lethal MDS in mice, and mechanistic studies showed that Setd2 catalyzing the K17me1 and K65me2 methylation modification of Srsf2P95H/+ protein, to inhibit the aberrant expression of Ceacam1-4 isoforms and inhibit the increased differentiation potential of HSPCs into MDSCs and the formation of Il-1β-related inhibitory tumor microenvironment. Overall, our findings proposed the possibility of targeting the CEACAM1-4- IL-1β signaling axis in the clinical treatment of SRSF2P95H/+ MDS patients
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 GSE265871_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 beta-value tables or raw IDAT files among the supplementary files.

Also filed as BioProject PRJNA1104591 and SRA study SRP504130. Searching any of these in the dataset finder brings you back here.

Study design
13 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 13 sample titles: 13 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
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