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(ChIP-seq-SHSY5Y) Hao-Fountain syndrome protein USP7 mediates neuronal differentiation via BCOR-ncPRC1.1

GSE263491 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2025/03/12 Platform GPL16791
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 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
Homo sapiens (human)
Samples
12 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
Hao-Fountain syndrome protein USP7 controls neuronal differentiation via BCOR-ncPRC1.1Genes & development · 2025
Summary (written by the submitters)
Pathogenic variants of ubiquitin-specific protease 7 (USP7) cause the neurodevelopmental disorder Hao-Fountain syndrome. However, which of its pleiotropic substrates are relevant for neurodevelopment has remained unclear. Here, we present a combination of quantitative proteomics, transcriptomics and epigenomics to define the core USP7 circuitry during neurodifferentiation.
Read the full summary ↓
USP7 activity is required for the transcriptional programs that direct the differentiation of human ESCs to neural stem cells, and neuronal differentiation of SHSY5Y neuroblastoma cells. In addition to other substrates, including TRIM27, USP7 controls the dosage of the Polycomb H2AK119ub1 ubiquitin ligases ncPRC1.1 and ncPRC1.6. We found that BCOR-ncPRC1.1, but not ncPRC1.6 or TRIM27, is a key effector of USP7-dependent neuronal differentiation. Indeed, BCOR-ncPRC1.1 mediates the majority of USP7-dependent gene regulation during this process. Besides providing a detailed map of the USP7 regulome during neuronal differentiation, our results suggest that Hao-Fountain syndrome and ncPRC1.1-associated neurodevelopmental disorders involve dysregulation of a shared epigenetic network.
Published in
Hao-Fountain syndrome protein USP7 controls neuronal differentiation via BCOR-ncPRC1.1
Wolf van der Meer J, Larue A, van der Knaap JA et al. · Genes & development 2025 · PMID 39919828 · doi:10.1101/gad.352272.124
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 GSE263491_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 PRJNA1097640 and SRA study SRP500331. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
WT_DIF_BCOR ×2 WT_FT671_DIF_BCOR ×2 WT_DIF_H2AK119Ub ×2 WT_FT671_DIF_H2AK119Ub ×2 WT_DIF_H3K27me3 ×2 WT_FT671_DIF_H3K27me3 ×2

Supports a between-group comparison across 12 samples.

How we read this: 6 replicated groups read from 12 sample titles; they account for 12 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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