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AMPK signaling downstream of adenosine 2A receptor represses Th17 cell pathogenicity through epigenetic and metabolic reprogramming.

GSE284714 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 15 samples Submitted 2025/09/27 Platform GPL30172Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 15 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
Mus musculus (mouse)
Samples
15 samples: 2 × PBS_Input_exp vs 2 × PBS_IP_H3K9ac_exp vs 2 × ActA_Input_exp vs 2 × ActA_IP_H3K9ac_expGroups 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
Adenosine 2A receptor-dependent activation of AMPK represses T(H)17 cell pathogenicity through epigenetic and metabolic reprogrammingScience signaling · 2025
Summary (written by the submitters)
Metabolic reprogramming controls protective or pathogenic Th17 cell responses; still, the precise molecular pathways that drive distinct immunometabolic states remain elusive. Here, we demonstrate that non-pathogenic Th17 cells induced by the immunoregulatory cytokine activin- A display reduced aerobic glycolysis and increased oxidative phosphorylation (OXPHOS).
Read the full summary ↓
Notably, signaling through the adenosine A 2A receptor (A 2A R)/AMP-activated protein kinase (AMPK) axis in response to activin-A, boosts OXPHOS and reprograms pathogenic Th17 cells towards non-pathogenic states. Epigenetic studies revealed that pathogenic Th17 cells express highly the CBP/P300 binding protein (PCAF) which facilitates the acetylation of histone 3 at lysine 9 (H3K9ac) at genes related to the mammalian target of rapamycin complex 1 (mTORC1), glycolysis and Th17 pathogenicity programs. Instead, activin-A-treated Th17 cells display an AMPK-mediated suppression of PCAF activity and aerobic metabolism while, accumulate H3K9ac in gene loci related to OXPHOS. Collectively, we uncover A 2A R-AMPK as a central metabolic checkpoint that epigenetically regulates Th17 pathogenicity.
Published in
Adenosine 2A receptor-dependent activation of AMPK represses T(H)17 cell pathogenicity through epigenetic and metabolic reprogramming
Papadopoulou G, Valakos D, Polydouri I et al. · Science signaling 2025 · PMID 40986641 · doi:10.1126/scisignal.adr3177
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 GSE284714_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 PRJNA1200091 and SRA study SRP552443. Searching any of these in the dataset finder brings you back here.

Study design
2 × PBS_Input_exp vs 2 × PBS_IP_H3K9ac_exp vs 2 × ActA_Input_exp vs 2 × ActA_IP_H3K9ac_exp

Supports a between-group comparison across 8 samples.

How we read this: 4 replicated groups read from 15 sample titles; they account for 8 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
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