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Nup153 regulates neuronal responsiveness through HDAC1-mediated epigenetic modulation [ChIP-seq]

GSE275917 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 17 samples Submitted 2026/07/31 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 17 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
17 samples: 7 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.
Summary (written by the submitters)
Neural activity-dependent gene regulation is central to the development of neural networks and neuronal plasticity. Induction of activity-dependent gene programs is equally important as repression of these programs, and both need to be balanced carefully. However, little is known about how repressive mechanisms modulate neuronal responsiveness across the genome before stimulation.
Read the full summary ↓
Here, we identify nucleoporin-dependent regulation of neuronal responsiveness in which Nup153 represses neuronal genes including activity-regulated genes (ARGs) in the basal state. By characterizing the genome-wide landscape of chromatin accessibility, histone modifications and Nup153 chromatin binding, we show that Nup153 directly influences their target genes and associated chromatin states through both basal activity-dependent and -independent mechanisms. Mechanistically, Nup153 recruits HDAC1 to regulate histone acetylation and repress target chromatin regions. We propose that Nup153 acts as a structural platform to recruit epigenetic repressor to maintain activity-dependent programs in the poised state, thus maintaining neuronal responsiveness as a gatekeeper.
This dataset
Open GSE275917 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 GSE275917_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 PRJNA1152568 and SRA study SRP528678. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
7 conditions, mostly in duplicate
CHIP_Basal_HDAC1 ×2 CHIP_Basal_Input ×2 CHIP_H3K27ac_Basal_shControl ×2 CHIP_H3K27ac_Basal_shNup153_2 ×2 CHIP_Input_Basal_shNup153_2 ×2 CHIP_H3K27ac_TTX_AP5_shControl ×2 CHIP_H3K27ac_TTX_AP5_shNup153_2 ×2 CHIP_Input_Basal_shControl ×1 +2 more

Supports a between-group comparison across 14 samples.

How we read this: 7 replicated groups read from 17 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
Datasets on a similar topic

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