GEO series

Phosphorylation of serines 287/288 in DEK regulates cell-type-specific chromatin occupancy and compaction [ChIP-Seq]

GSE324916 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 24 samples Submitted 2026/03/21 Platform GPL23227

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 24 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: MelanomaThis series is part of our curated briefing on it.
Samples: 24 samples: 24 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)

The conserved multifunctional chromatin modulator and oncogene DEK exhibits context-dependent genomic binding and function, but how these activities are regulated in cancer remains poorly understood. Using multi-omics and biochemical approaches, we find that while DEK predominantly occupies promoter-proximal regions in HeLa cells and primary melanocytes, its chromatin binding is dramatically reduced in melanoma cell lines—despite DEK overexpression.

Read the full summary ↓

We attributed this to CK2-mediated phosphorylation, which governs DEK chromatin association and transcriptional output in a cell-type-specific manner. Phosphoproteomics identified 34 phosphorylation sites, including S287 and S288 within the DEK C-terminal DNA-binding domain. Strikingly, CK2 inhibition and concomitant loss of phosphorylation at S287/S288 triggered DEK redistribution to promoter regions, coinciding with transcriptional repression of oncogenic pathways and global chromatin compaction. Melanoma subtypes showed divergent responses: NRAS-mutant cells displayed dynamic, phosphorylation-dependent DEK redistribution, whereas BRAF-mutant cells lacked detectable DEK binding. Our work establishes DEK as a phosphorylation-sensitive regulator of chromatin states, with CK2-mediated modification orchestrating its tumor-specific regulatory functions. These findings nominate phospho-DEK as a potential biomarker and therapeutic target in melanoma and possibly other cancers.

This dataset

Open GSE324916 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Melanoma 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 GSE324916_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 PRJNA1438081 and SRA study SRP684034. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

24 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 24 sample titles: 24 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

GSM9588803 SK-Mel-103, CX-4945 treatment, DEK, replicate 1 (ChIP)
GSM9588804 SK-Mel-103, CX-4945 treatment, DEK, replicate 2 (ChIP)
GSM9588805 SK-Mel-103, CX-4945 treatment, DEK, replicate 3 (ChIP)
GSM9588806 SK-Mel-103, CX-4945 treatment, DEK, replicate 1 (Input)
GSM9588807 SK-Mel-103, CX-4945 treatment, DEK, replicate 2 (Input)
GSM9588808 SK-Mel-103, CX-4945 treatment, DEK, replicate 3 (Input)
GSM9588809 SK-Mel-103, DMSO treatment, DEK, replicate 1 (ChIP)
GSM9588810 SK-Mel-103, DMSO treatment, DEK, replicate 2 (ChIP)
GSM9588811 SK-Mel-103, DMSO treatment, DEK, replicate 3 (ChIP)
GSM9588812 SK-Mel-103, DMSO treatment, DEK, replicate 1 (Input)
GSM9588813 SK-Mel-103, DMSO treatment, DEK, replicate 2 (Input)
GSM9588814 SK-Mel-103, DMSO treatment, DEK, replicate 3 (Input)
GSM9588815 HeLa S3, DEK, replicate 1 (ChIP)
GSM9588816 HeLa S3, DEK, replicate 2 (ChIP)
GSM9588817 HeLa S3, DEK, replicate 3 (ChIP)
GSM9588818 HeLa S3, DEK, replicate 1 (Input)
GSM9588819 HeLa S3, DEK, replicate 2 (Input)
GSM9588820 HeLa S3, DEK, replicate 3 (Input)
GSM9588821 FM232, DEK, replicate 1 (ChIP)
GSM9588822 FM232, DEK, replicate 2 (ChIP)
GSM9588823 FM232, DEK, replicate 3 (ChIP)
GSM9588824 FM232, DEK, replicate 1 (Input)
GSM9588825 FM232, DEK, replicate 2 (Input)
GSM9588826 FM232, DEK, replicate 3 (Input)

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Search all human ChIP / ATAC / CUT&Tag datasets in GEO →

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