Autoimmune Disease Risk Gene ANKRD55 Promotes Th17 Effector Function Through Metabolic Modulation [ATAC-Seq]
ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 36 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
- 36 samples: 18 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
- Autoimmune disease risk gene ANKRD55 promotes TH17 effector function through metabolic modulationThe Journal of experimental medicine · 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 GSE303700_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 PRJNA1297113 and SRA study SRP603705. Searching any of these in the dataset finder brings you back here.
Supports a between-group comparison across 36 samples.
How we read this: 18 replicated groups read from 36 sample titles; they account for 36 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.
- GSM9134322 Th0_KO1_S22 Th0_KO1_S
- GSM9134323 Th0_KO1_S4 Th0_KO1_S
- GSM9134324 Th0_KO2_S23 Th0_KO2_S
- GSM9134325 Th0_KO2_S5 Th0_KO2_S
- GSM9134326 Th0_KO3_S24 Th0_KO3_S
- GSM9134327 Th0_KO3_S6 Th0_KO3_S
- GSM9134328 Th0_WT1_S19 Th0_WT1_S
- GSM9134329 Th0_WT1_S1 Th0_WT1_S
- GSM9134330 Th0_WT2_S20 Th0_WT2_S
- GSM9134331 Th0_WT2_S2 Th0_WT2_S
- GSM9134332 Th0_WT3_S21 Th0_WT3_S
- GSM9134333 Th0_WT3_S3 Th0_WT3_S
- GSM9134334 Th17n_KO1_S10 Th17n_KO1_S
- GSM9134335 Th17n_KO1_S28 Th17n_KO1_S
- GSM9134336 Th17n_KO2_S11 Th17n_KO2_S
- GSM9134337 Th17n_KO2_S29 Th17n_KO2_S
- GSM9134338 Th17n_KO3_S12 Th17n_KO3_S
- GSM9134339 Th17n_KO3_S30 Th17n_KO3_S
- GSM9134340 Th17n_WT1_S25 Th17n_WT1_S
- GSM9134341 Th17n_WT1_S7 Th17n_WT1_S
- GSM9134342 Th17n_WT2_S26 Th17n_WT2_S
- GSM9134343 Th17n_WT2_S8 Th17n_WT2_S
- GSM9134344 Th17n_WT3_S27 Th17n_WT3_S
- GSM9134345 Th17n_WT3_S9 Th17n_WT3_S
- GSM9134346 Th17p_KO1_S16 Th17p_KO1_S
- GSM9134347 Th17p_KO1_S34 Th17p_KO1_S
- GSM9134348 Th17p_KO2_S17 Th17p_KO2_S
- GSM9134349 Th17p_KO2_S35 Th17p_KO2_S
- GSM9134350 Th17p_KO3_S18 Th17p_KO3_S
- GSM9134351 Th17p_KO3_S36 Th17p_KO3_S
- GSM9134352 Th17p_WT1_S13 Th17p_WT1_S
- GSM9134353 Th17p_WT1_S31 Th17p_WT1_S
- GSM9134354 Th17p_WT2_S14 Th17p_WT2_S
- GSM9134355 Th17p_WT2_S32 Th17p_WT2_S
- GSM9134356 Th17p_WT3_S15 Th17p_WT3_S
- GSM9134357 Th17p_WT3_S33 Th17p_WT3_S
- GSE303699 Autoimmune Disease Risk Gene ANKRD55 Promotes Th17 Effector Function Through Metabolic Modulation [RNA-Seq] 60 samples shares ankrd55, th17, autoimmune, modulation, promotes, effector, risk
- GSE233905 Transcription factor TCF1 binds Rorgt and orchestrates a regulatory network that determines homeostatic Th17 cell state [ATAC-seq] 13 samples shares th17, atac-seq
- GSE320348 A cell-intrinsic glucocorticoid biosynthesis and sensing circuit maintains homeostatic Th17 cell state [ATAC-seq] 12 samples shares th17, atac-seq
- GSE296200 A20’s Linear Ubiquitin Binding Motif Restrains Pathogenic Activation of TH17/22 cells and IL-22 Driven Enteritis [ATAC-seq] 11 samples shares th17, atac-seq
- 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, atac-seq
- GSE296401 Interleukin-23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity II 38 samples shares th17, promotes
- GSE298131 Gut microbe-derived metabolites drive psoriatic inflammation via modulation of skin Th17 cells 18 samples shares th17, modulation
- GSE285450 Fructose specifically exacerbates pathogenic-Th17 cell differentiation and autoimmune diseases through ROS-EGFR signal 18 samples shares th17, autoimmune
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.