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Interferons promote autophagy via the STAT1/STAT5B-SOCS1 axis

GSE302359 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2026/07/01 Platform GPL30173
At a glance

RNA-seq (gene expression) · human · 12 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
12 samples: 3 × HeLa GL cells, control, vs 3 × HeLa GL cells, STAT5Inh, vs 3 × HeLa GL cells, IFNb, vs 3 × HeLa GL cells, STAT5Inh+IFNb,Groups 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)
Concerted activation of the interferon (IFN) system and autophagy upon viral infection is paramount for efficient immune defences. Here, we show that IFN activates autophagy via STAT1/5B heterodimer-mediated upregulation of SOCS1 and contributes to virus-induced autophagy. Our data demonstrate that autophagic flux activation by type I and II IFNs peaks at 24 h post treatment, whereas type III IFNs induce autophagy with slower kinetics.
Read the full summary ↓
Mechanistically, IFN-mediated autophagy induction is dependent on JAK1-3 and both STAT1 as well as STAT5B. We show that STAT1 and STAT5B form heterodimers and co-localize following IFN treatment. Transcriptome analyses revealed that SOCS1 is induced in a STAT5B-dependent manner, and depletion of SOCS1 prevented IFN-induced autophagy. Finally, pharmacological inhibition of STAT5B or scavenging of IFN diminishes autophagosome levels upon infection with Sendai, respiratory syncytial, measles and influenza A viruses. Taken together, our data indicate that the IFN system and autophagy are connected via the STAT1/STAT5B-SOCS1 axis and that this axis is required for concerted activation of both systems during viral infections. Targeting of this signalling axis may allow to boost autophagy against viral infections.
This dataset
Open GSE302359 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 GSE302359_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 PRJNA1290249 and SRA study SRP600096. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
3 × HeLa GL cells, control, vs 3 × HeLa GL cells, STAT5Inh, vs 3 × HeLa GL cells, IFNb, vs 3 × HeLa GL cells, STAT5Inh+IFNb,

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.