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Revealing an unconventional JAK1/2-STAT3 branch in macrophage IFNγ signaling [RNA-Seq]

GSE304588 Mus musculus (mouse) RNA-seq (gene expression) 30 samples Submitted 2025/12/23 Platform GPL34290
At a glance

RNA-seq (gene expression) · mouse · 30 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
Mus musculus (mouse)
Samples
30 samples: 15 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.
Paper
Revealing an unconventional JAK1/2-STAT3 branch in macrophage IFN-γ signalingCell reports · 2026
Summary (written by the submitters)
Interferon-γ (IFNγ) is a key cytokine in immune activation and anti-viral responses that classically signals via JAK1/2-mediated STAT1 homodimers to drive macrophage activation. Here, we identify a non-canonical signaling component in which IFNγ also activates STAT3. Our results show that IFNγ activates STAT3 rapidly and directly through JAK1 and JAK2.
Read the full summary ↓
We provide the first evidence that STAT3 can form heterodimers with STAT1 in this context and demonstrate that STAT3 is co-recruited to a subset of IFNγ-induced, STAT1-bound regulatory elements. While IFNγ directly activates STAT3, our results reveal that its contribution to gene regulation is limited, indicating that STAT1 easily substitutes the STAT1–STAT3 heterodimer for STAT1 homodimers when STAT3 is absent. These findings uncover STAT3 as a new unconventional player in macrophage IFNγ signaling, underscoring the complex and context-dependent nature of cytokine signaling networks.
Published in
Revealing an unconventional JAK1/2-STAT3 branch in macrophage IFN-γ signaling
Botman M, Huisman JMA, Drakaki A et al. · Cell reports 2026 · PMID 41671082 · doi:10.1016/j.celrep.2026.116985
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 GSE304588_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: 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 PRJNA1301842 and SRA study SRP606853. Searching any of these in the dataset finder brings you back here.

Study design
15 conditions, mostly in duplicate
STAT1WT_Ctrl_2h ×2 STAT1WT_IFNg_2h ×2 STAT1KO_Ctrl_2h ×2 STAT1KO_IFNg_2h ×2 STAT3WT_Ctrl_2h ×2 STAT3WT_IFNg_2h ×2 STAT3KO_Ctrl_2h ×2 STAT3KO_IFNg_2h ×2 +7 more

Supports a between-group comparison across 30 samples.

How we read this: 15 replicated groups read from 30 sample titles; they account for 30 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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