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Negative regulation of TH17-mediated inflammation by the nuclear receptor REV-ERBβ

GSE317634 Mus musculus (mouse) RNA-seq (gene expression) 26 samples Submitted 2026/03/27 Platform GPL19057
At a glance

RNA-seq (gene expression) · mouse · 26 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
26 samples: 13 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.
Summary (written by the submitters)
TH17 cells play a central role in several human autoimmune diseases. We and others reported the nuclear receptor REV-ERBα as a cell-intrinsic repressor of TH17-mediated pathogenicity. REV-ERBβ, REV-ERBα’s closely related family member, is thought to be functionally redundant to REV-ERBα, which we sought to explore in TH17-mediated immunity.
Read the full summary ↓
Our data indicate that deletion of REV-ERBβ enhanced TH17-mediated pro-inflammatory cytokine expression and exacerbated disease in mouse models of multiple sclerosis and colitis. RNA-sequencing indicates REV-ERBβ and REV-ERBα do not have similar transcriptional profiles. REV-ERBβ does not appear to regulate gene expression through interaction with the classic co-repressor NCoR1, which is in contrast to REV-ERBα in TH17 cells, nor does it utilize heme, its known endogenous ligand for its repressive functions. Our results establish that while REV-ERBβ also acts as a negative regulator of TH17-cell function and pathogenicity, it does so in a manner that is non-redundant, independent, and unique to REV-ERBα.
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 GSE317634_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 PRJNA1414575. Searching any of these in the dataset finder brings you back here.

Study design
13 conditions, mostly in duplicate
CD4 T cell, REV-Erbβ WT, 0hr, ×2 CD4 T cell, REV-Erbβ KO, 0hr, ×2 CD4 T cell, REV-Erbβ WT, 24hr, ×2 CD4 T cell, REV-Erbβ KO, 24hr, ×2 CD4 T cell, REV-Erbα WT, 0hr, ×2 CD4 T cell, REV-Erbα KO, 0hr, ×2 CD4 T cell, REV-Erbα WT, 24hr, ×2 CD4 T cell, REV-Erbα KO, 24hr, ×2 +5 more

Supports a case/control comparison: 8 samples read as cases, 8 as controls.

How we read this: 13 replicated groups read from 26 sample titles; they account for 26 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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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.