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Menin orchestrates corticogenesis via epigenetic activation of EphA4 in late-born neurons

GSE296891 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/08/01 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 12 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
12 samples: 12 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)
The development of the mammalian cerebral cortex is tightly regulated by epigenetic mechanisms. However, the role of epigenetic modifications in gene regulation and their impact on neocortical function remain poorly understood. Here, we demonstrate that Menin, encoded by the multiple endocrine neoplasia type 1 (Men1) gene, is essential for neurogenesis.
Read the full summary ↓
Deficiency in Men1 disrupts the formation of the laminated neocortex, particularly in the upper-layer neurons. In Men1-deficient late-born neurons, migration to their final positions is impaired, accompanied by defective neuronal polarization. Mechanistic studies reveal that Menin regulates global chromatin accessibility at transcriptional start sites of genes critical for neuronal development. The loss function of Menin primarily reduces H3K4me3 deposition at promoter regions. Notably, complementation with EphA4 in late-born neurons mitigates polarization defects in the context of Men1 deficiency. These findings support the importance of Menin in corticogenesis, providing insight into the formation of the cerebral cortex.
This dataset
Open GSE296891 in finder → Find more mouse 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 GSE296891_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 PRJNA1261890 and SRA study SRP584760. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
12 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 12 sample titles: 12 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
Datasets on a similar topic

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