Stress-Induced Glucocorticoids Exacerbate Inflammation and Autoimmunity by Promoting the Differentiation and Function of Th17 Cells [ChIP-seq]
ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 3 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
- 3 samples
- 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
- Stress-induced glucocorticoids enhance acute inflammation by promoting the differentiation of Th17 cellsCell reports · 2025
Read the full summary ↓
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.
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.
Supplementary files
The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE235250_RAW.tar (it can run to tens of gigabytes).
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 PRJNA985615 and SRA study SRP444818. Searching any of these in the dataset finder brings you back here.
The sample list for this study is not cached yet. Press Load samples and it will be fetched from NCBI.
+ 3 more — browse all 3 samples with per-sample file links →
- GSE285450 Fructose specifically exacerbates pathogenic-Th17 cell differentiation and autoimmune diseases through ROS-EGFR signal 18 samples shares th17, exacerbate
- GSE298306 Immune-responsive gene-1: The mitochondrial Key to Th17 Cell Pathogenicity in CNS Autoimmunity 18 samples shares th17, autoimmunity
- GSE326921 The chromatin assembly factor CHAF1b functions as an epigenetic amplifier of RORγt to promote Th17 pathogenicity and autoimmunity 13 samples shares th17, autoimmunity
- GSE250576 ATAC-seq of Satb1 conditional KO in CD4+ naïve T cells reveals epigenetic role of Satb1 in developing Th17 T cells by controlling the accessibility of Il2, thereby inhibiting IL-2 signaling in the initial stages of T cell differentiation. 10 samples shares th17
- GSE267422 Myelin-reactive B cells exacerbate the severity of CD4+ T cell-driven CNS autoimmunity in an IL-23-dependent manner 12 samples shares autoimmunity, exacerbate
- GSE303700 Autoimmune Disease Risk Gene ANKRD55 Promotes Th17 Effector Function Through Metabolic Modulation [ATAC-Seq] 36 samples shares th17
- GSE254602 Effect of deletion of SPTLC1 on gene expression and differentiation of mouse Th17 cells in vitro 24 samples shares th17
- GSE250579 Satb1 directs the differentiation of TH17 cells through suppression of IL-2 expression 20 samples shares th17
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.