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H3 dopaminylation and CaMKII modulate diffuse midline glioma response to CDK9 inhibition

GSE324146 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 50 samples Submitted 2026/04/23 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 50 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
50 samples: 19 conditions, mostly in triplicateGroups 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
H3 dopaminylation and CaMKII modulate diffuse midline glioma response to CDK9 inhibitionbioRxiv : the preprint server for biology · 2026
Summary (written by the submitters)
Aberrant neurotransmitter signaling and transcriptional dysregulation are hallmarks of gliomagenesis and represent potential therapeutic targets. Monoamine neurotransmitters such as dopamine and serotonin primarily activate GPCRs but can also function epigenetically as histone H3 modifications. Here, we uncover mechanisms of crosstalk between monoamine neurotransmitter signaling, H3 dopaminylation, and RNA polymerase II (Pol2) transcription in diffuse midline glioma (DMG).
Read the full summary ↓
We find that co-treatment with Pol2 targeting CDK9 inhibitors (CDK9i) and FDA approved neuropsychiatric drugs, including selective serotonin reuptake inhibitors (SSRIs), synergistically reduces DMG growth. Mechanistically, CDK9i+SSRI treatment alters H3 dopaminylation patterns and represses synaptic and neurodevelopmental gene transcription associated with CDK9i resistance. Further phospho-proteomic analyses show that CDK9i monotherapy activates pro survival CaMKII signaling, which can be suppressed by co-treatment with neuromodulatory drugs. These studies establish roles for H3 dopaminylation and neurotransmitter signaling in DMG gene regulation and response to CDK9i, suggesting that monoamine neurotransmitter pathways may be exploited as a therapeutic strategy for DMG. This SuperSeries is composed of the SubSeries listed below.
Published in
H3 dopaminylation and CaMKII modulate diffuse midline glioma response to CDK9 inhibition
Murdaugh RL, Eberl BR, Richard RU et al. · bioRxiv : the preprint server for biology 2026 · PMID 41993356 · doi:10.64898/2026.04.07.714507
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 GSE324146_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 PRJNA1433516 and SRA study SRP665686. Searching any of these in the dataset finder brings you back here.

Study design
19 conditions, mostly in triplicate
DIPGXIII, DMSO, 24hr, ×3 DIPGXIII, zotiraciclib+sertraline, 24hr, ×3 DIPGXIIIP*xenograft, DMSO, ×3 DIPGXIIIP*xenograft, zotiraciclib, ×3 DIPGXIII, DMSO, ×3 DIPGXIII, AZD4573, ×3 DIPGXIII, zotiraciclib, ×3 DIPGXIII, sertraline, ×3 +13 more

Supports a between-group comparison across 48 samples.

How we read this: 19 replicated groups read from 50 sample titles; they account for 48 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

+ 10 more — browse all 50 samples with per-sample file links →

Datasets on a similar topic

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