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Co-targeting neurotransmitter signaling and CDK9 to treat diffuse midline glioma [RNA-seq]

GSE317726 Homo sapiens (human) RNA-seq (gene expression) 24 samples Submitted 2026/04/24 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 24 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Samples
24 samples: 8 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 glioma and represent potential therapeutic targets. In this study, we uncover mechanisms of crosstalk between monoamine neurotransmitter signaling and transcriptional regulation in diffuse midline glioma (DMG) that can be co-targeted with CDK9 inhibitors (CDK9i) and neuropsychiatric drugs as a potential treatment strategy for DMG.
Read the full summary ↓
We identified compounds that synergize with CDK9i in DMG using targeted drug screens, then assessed DMG response to CDK9i and neurotransmitter-targeting drugs in cell culture and in orthotopic xenograft mouse models. We then used a multi-omic approach combining proteomic, transcriptomic, and chromatin profiling with phospho-proteomics, RNA-seq, CUT&RUN, and ATAC-seq in DMG cells to characterize mechanisms of synergy between CDK9i and neuropsychiatric drugs. We observe differential expression of neuronal signaling genes in both CDK9i-resistant DMG xenograft tumors and CDK9-low pediatric high grade glioma patient tumors. Additional studies reveal that drugs that modify monoamine neurotransmitter signaling, including neurotransmitter reuptake inhibitors (SSRI/SNRI) and both metabotropic neurotransmitter receptor agonists and antagonists, strongly synergize with CDK9i to reduce DMG cell viability. Co-treating DMG with CDK9i+SSRI/SNRI triggered negative feedback inhibition of autocrine neurotransmitter receptor signaling and reversed a CAMKII-dependent mechanism of CDK9i resistance. Finally, we find that CDK9i+SSRI resulted in altered histone dopaminylation at neurodevelopmental genes associated with CDK9i-resistance. These findings identify neurotransmitter signaling pathways as novel points of vulnerability in CDK9i-resistant DMG that can be targeted with FDA-approved psychiatric drugs to modulate CAMKII signaling and histone dopaminylation in pediatric brain tumors.
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
Open GSE317726 in finder → Find more human RNA-seq datasets →
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 GSE317726_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1415112 and SRA study SRP667754. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41993356) ↗
Study design
8 conditions, mostly in triplicate
DIPGXIIIP*xenograft, DMSO, ×3 DIPGXIIIP*xenograft, zotiraciclib, ×3 DIPGXIII, DMSO, ×3 DIPGXIII, AZD4573, ×3 DIPGXIII, zotiraciclib, ×3 DIPGXIII, sertraline, ×3 DIPGXIII, AZD4573+sertraline, ×3 DIPGXIII, zotiraciclib+sertraline, ×3

Supports a between-group comparison across 24 samples.

How we read this: 8 replicated groups read from 24 sample titles; they account for 24 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
Datasets on a similar topic

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