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CDK8 inhibition sequesters Med1 at EWS-FLI enhancers [ChIP-seq]

GSE302426 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 22 samples Submitted 2026/07/09 Platform GPL24676Platform GPL30173
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 22 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
Ewing sarcomaThis series is part of our curated briefing on it.
Samples
22 samples: 8 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)
Ewing sarcoma is characterized by a chromosomal translocation resulting in the fusion protein EWSR1-FLI1. To identify small molecules that selectively impair the oncogenic transcriptional program enacted by EWS-FLI1 we employed a novel phenotypic screen. Our screening hits were enriched for inhibitors of cyclin dependent kinase 8/19.
Read the full summary ↓
Inhibition of CDK8/19 resulted in a proliferation defect in Ewing sarcoma cells and a reduction in growth of Ewing sarcoma xenografts. We performed a genome wide pooled CRISPR screen that suggested that small molecule inhibition of CDK8/19 acted in a gain-of-function manner that did not replicate the effects of CDK8/19 genetic knockout. Through biochemical studies and chromatin profiling, we discovered that CDK8/19 inhibitors act through a novel trapping mechanism in which the inhibitor prevents dissociation of the CDK8 kinase from core Mediator. This mechanism has broad implications for the development of small molecules to target transcriptional regulation.
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 GSE302426_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 PRJNA1290400 and SRA study SRP600263. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly in duplicate
A673_EWSFLI-AID_NChIP-H3K27ac_DMSO ×2 A673_EWSFLI-AID_NChIP-H3K27ac_IAA ×2 A673_NChIP-H3K27ac_DMSO ×2 A673_NChIP-H3K27ac_SW39 ×2 A673_XChIP-MED1_DMSO ×2 A673_XChIP-MED1_SW39 ×2 A673_NChIP-H3K9ac_DMSO ×2 A673_NChIP-H3K9ac_SW39 ×2 +6 more

Supports a between-group comparison across 16 samples.

How we read this: 8 replicated groups read from 22 sample titles; they account for 16 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
More Ewing sarcoma 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.