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YAPTAZ and neuroblastoma cell plasticity [ChIP-seq]

GSE292597 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 29 samples Submitted 2026/05/10 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 29 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
29 samples: 29 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)
High-risk neuroblastoma is a pediatric malignancy marked by poor prognosis, high metastatic potential, and resistance to conventional therapies. Phenotypic plasticity between noradrenergic and mesenchymal cell states, each defined by specific transcriptional and epigenetic programs and distinct cellular properties, is observed in some neuroblastoma cell lines.
Read the full summary ↓
Yet the drivers of this plasticity are not fully understood. This study identifies YAP and TAZ as central regulators of the mesenchymal state. YAP/TAZ, in complex with TEAD, FOSL, and RUNX transcription factors, establish a core regulatory circuitry associated with mesenchymal-specific super-enhancers. Expression of a conserved YAP/TAZ gene signature increases during the noradrenergic-to-mesenchymal transition and decreases during the reverse in plasticity models. Genetic or pharmacological inactivation of YAP/TAZ abrogates cellular proliferation and inhibits the noradrenergic-to-mesenchymal transition. Conversely, overexpression of YAP/TAZ in noradrenergic cells induces a major transcriptional reprogramming towards a mesenchymal state, via a redistribution of TEAD4 and a rewiring of the epigenetic landscape. These findings uncover a YAP/TAZ-TEAD4 driven epigenetic mechanism underlying tumor cell plasticity in neuroblastoma.
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 GSE292597_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 PRJNA1240277 and SRA study SRP572220. Searching any of these in the dataset finder brings you back here.

Study design
29 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 29 sample titles: 29 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
More Neuroblastoma datasets

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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.