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RUVBL1 and RUVBL2 are druggable MYCN regulators in neuroblastoma

GSE312769 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 13 samples Submitted 2025/12/22 Platform GPL30173
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 13 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)
Topic
NeuroblastomaThis series is part of our curated briefing on it.
Samples
13 samples: 3 × BAR_IgG vs 3 × BAR_H3K27ac vs 3 × BAR_MYCN vs 3 × BAR_RUVBL2Groups 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)
High-risk neuroblastoma (NB), accounting for approximately 50% of all cases, exhibits high relapse rates and life-threatening toxicities despite intensive therapies, highlighting the need for safer and more effective treatments. Analysis of publicly available NB transcriptomic datasets identified RUVBL2 as a key node in the MYC(N) regulatory network.
Read the full summary ↓
High MYC signature scores were observed in high-risk NB cohorts, and multivariate Cox regression analysis showed that RUVBL1/2 expression is an independent predictor of both overall and event-free survival. Experimental validation through cell culture, western blotting, qPCR, and RNA-seq demonstrated that knockdown or pharmacological inhibition of RUVBL1/2 using CB-6644 induced replication stress, leading to cell cycle arrest, DNA damage, and apoptosis. Mechanistically, RUVBL1/2 regulated ATR and ATM protein stability and transcriptionally controlled MYC(N) expression. These findings indicate that RUVBL1 and RUVBL2 are novel regulators of the DNA damage response with both therapeutic and prognostic potential in high-risk NB.
This dataset
Open GSE312769 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Neuroblastoma landscape →
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 GSE312769_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 PRJNA1375842 and SRA study SRP651854. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
3 × BAR_IgG vs 3 × BAR_H3K27ac vs 3 × BAR_MYCN vs 3 × BAR_RUVBL2

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 13 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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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.