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A nuclear ERK–ATF5 axis coordinates mitochondrial metabolism and thermogenic gene expression in brown adipocytes

GSE315093 Mus musculus (mouse) RNA-seq (gene expression) 10 samples Submitted 2026/05/31 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 10 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
10 samples: 8 distinct titles, 2 of them repeatedGroups 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)
Obesity and diabetes result from disrupted energy homeostasis, highlighting the importance of identifying molecular mechanisms that enhance energy expenditure. Brown adipose tissue (BAT) dissipates energy through mitochondria-dependent non-shivering thermogenesis, yet the transcriptional regulators coordinating this process remain incompletely defined.
Read the full summary ↓
In this study, we identify activating transcription factor 5 (ATF5) as a key regulator of thermogenic gene expression and mitochondrial metabolism in brown adipocytes. Cold exposure and β3-adrenergic stimulation robustly induced Atf5 expression in BAT and differentiated brown adipocytes, coinciding with activation of canonical thermogenic programs. Mechanistically, ATF5 functions downstream of a nuclear PKA–ERK signaling axis, where nuclear ERK1/2 activation is required for ATF5 induction and subsequent upregulation of UCP1. Loss of Atf5 impaired thermogenic transcription, suppressed mitochondrial unfolded protein response (UPRmt) and lipolytic gene expression, and reduced mitochondrial oxidative capacity and metabolic flexibility. Transcriptomic profiling revealed broad downregulation of fatty acid oxidation, β-oxidation, oxidative phosphorylation, and thermogenic pathways in Atf5-deficient brown adipocytes. Collectively, these data establish ATF5 as a central transcriptional regulator that integrates mitochondrial metabolism, lipid catabolism, and thermogenic activation in brown adipocytes, providing mechanistic insight into energy expenditure regulation.
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 GSE315093_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 PRJNA1394982 and SRA study SRP658556. Searching any of these in the dataset finder brings you back here.

Study design
8 distinct titles, 2 of them repeated
BAT, control ×2 BAT, ATF5KO ×2

How we read this: Read from 10 sample titles: 8 distinct titles with little repetition. 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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