GEO series

Heterozygous Kmt2d loss diminishes enhancers to render medulloblastoma cells vulnerable to combinatory inhibition of lysine demethylation and oxidative phosphorylation [RNA-seq]

GSE293811 Mus musculus (mouse) DNA methylation 10 samples Submitted 2025/06/02 Platform GPL19057

At a glance

DNA methylation · mouse · 10 samples

What it is: DNA methylationChemical marks on DNA that help switch genes on or off.
Organism: Mus musculus (mouse)
Samples: 10 samples: 4 × Ptch, Cerebellum, Control, RNA-seq, vs 3 × NKP, Medulloblastoma, KO, RNA-seq, vs 3 × AKP, Medulloblastoma, KO, RNA-seq,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.

Summary (written by the submitters)

The histone methyltransferase KMT2D (alias MLL4) is frequently mutated in medulloblastoma (MB). Heterozygous loss of KMT2D is prevalent in MB. However, the role of heterozygous KMT2D loss remains unknown. Here, we show that heterozygous Kmt2d loss highly promotes Ptch+/–-driven MB genesis in mice. Heterozygous Kmt2d loss upregulated tumor-promoting programs, including oxidative phosphorylation (OXPHOS), in Ptch+/–-driven MB genesis.

Read the full summary ↓

Heterozygous Kmt2d loss extensively diminished enhancer signals and H3K4me3 signature, including those for transcription-repressive tumor suppressor genes (e.g., Ncor2). NCOR2 repressed the expression of tumor-promoting genes. Combinatory pharmacological inhibition of OXPHOS and the enhancer-decommissioning demethylase LSD1 drastically reduced the tumorigenicity of MB cells bearing heterozygous Kmt2d loss. These findings reveal the mechanistic basis underlying the MB-promoting effect of heterozygous KMT2D loss.

This dataset

Open GSE293811 in finder → Find more mouse RNA-seq 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 GSE293811_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 beta-value tables or raw IDAT files among the supplementary files.

Also filed as BioProject PRJNA1246494 and SRA study SRP576467. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

4 × Ptch, Cerebellum, Control, RNA-seq, vs 3 × NKP, Medulloblastoma, KO, RNA-seq, vs 3 × AKP, Medulloblastoma, KO, RNA-seq,

Supports a between-group comparison across 10 samples.

How we read this: 3 replicated groups read from 10 sample titles; they account for 10 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

GSM8890598 Ptch, Cerebellum, Control, RNA-seq, rep1 Ptch, Cerebellum, Contr…
GSM8890599 Ptch, Cerebellum, Control, RNA-seq, rep2 Ptch, Cerebellum, Contr…
GSM8890600 Ptch, Cerebellum, Control, RNA-seq, rep3 Ptch, Cerebellum, Contr…
GSM8890601 Ptch, Cerebellum, Control, RNA-seq, rep4 Ptch, Cerebellum, Contr…
GSM8890602 NKP, Medulloblastoma, KO, RNA-seq, rep1 NKP, Medulloblastoma, K…
GSM8890603 NKP, Medulloblastoma, KO, RNA-seq, rep2 NKP, Medulloblastoma, K…
GSM8890604 NKP, Medulloblastoma, KO, RNA-seq, rep3 NKP, Medulloblastoma, K…
GSM8890605 AKP, Medulloblastoma, KO, RNA-seq, rep1 AKP, Medulloblastoma, K…
GSM8890606 AKP, Medulloblastoma, KO, RNA-seq, rep2 AKP, Medulloblastoma, K…
GSM8890607 AKP, Medulloblastoma, KO, RNA-seq, rep3 AKP, Medulloblastoma, K…

Datasets on a similar topic

GSE248458 Heterozygous Kmt2d loss diminishes enhancers to render medulloblastoma cells vulnerable to combinatory inhibition of lysine demethylation and oxidative phosphorylation 25 samples shares kmt2d, medulloblastoma, phosphorylation, demethylation, heterozygous, combinatory, diminishes, vulnerable
GSE325800 KMT2C and KMT2D amplify GRHL2-driven enhancer activation [RNA-Seq] 30 samples shares kmt2d
GSE328371 KMT2D depletion promote KRAS-induced pancreatic carcinogenesis independent of TP53 24 samples shares kmt2d
GSE237287 Loss of Kmt2c or Kmt2d drives brain metastasis via KDM6A-dependent upregulation of MMP3 [RNA-seq] 18 samples shares kmt2d
GSE316994 Epigenetic and transcriptional alterations in Kmt2c/Kmt2d-deficient gastric cancer [RNA-seq] 12 samples shares kmt2d
GSE292432 Single cell RNA sequencing analysis following Kmt2c/Kmt2d and Pten knockout in mouse stomach mucosa. 10 samples shares kmt2d
GSE237289 Loss of Kmt2c or Kmt2d drives brain metastasis via KDM6A-dependent upregulation of MMP3 [scRNA-seq] 9 samples shares kmt2d
GSE290849 Acute intervention reveals critical roles of BAF, KMT2D and p300 in MyoD binding on enhancers 143 samples shares kmt2d

Search all mouse RNA-seq datasets in GEO →

Share this dataset

Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.