Neurons undergo IFNγ-driven persistent epigenetic shifts and synaptic remodeling in the inflamed brain [ChIP-Seq]
ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 57 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
- 57 samples: 21 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
- Neurons undergo IFNγ-driven persistent epigenetic shifts and synaptopathy in encephalitisNeuron · 2026
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 GSE289108_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 PRJNA1221548 and SRA study SRP562712. Searching any of these in the dataset finder brings you back here.
Supports a between-group comparison across 42 samples.
How we read this: 21 replicated groups read from 57 sample titles; they account for 42 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.
- GSM8783817 WT_CC10_H3K27ac_HC_rep1 WT_CC10_H3K27ac_HC
- GSM8783818 WT_CC10_H3K27ac_HC_rep2 WT_CC10_H3K27ac_HC
- GSM8783819 WT_CC10_H3K27me3_HC_rep1 WT_CC10_H3K27me3_HC
- GSM8783820 WT_CC10_H3K27me3_HC_rep2 WT_CC10_H3K27me3_HC
- GSM8783821 WT_CC10_H3K4me3_HC_rep1 WT_CC10_H3K4me3_HC
- GSM8783822 WT_CC10_H3K4me3_HC_rep2 WT_CC10_H3K4me3_HC
- GSM8783823 WT_CC30_H3K27ac_HC_rep1 WT_CC30_H3K27ac_HC
- GSM8783824 WT_CC30_H3K27ac_HC_rep2 WT_CC30_H3K27ac_HC
- GSM8783825 WT_CC30_H3K27me3_HC_rep1 WT_CC30_H3K27me3_HC
- GSM8783826 WT_CC30_H3K27me3_HC_rep2 WT_CC30_H3K27me3_HC
- GSM8783827 WT_CC30_H3K4me3_HC_rep1 WT_CC30_H3K4me3_HC
- GSM8783828 WT_CC30_H3K4me3_HC_rep2 WT_CC30_H3K4me3_HC
- GSM8783829 WT_CC70_H3K27ac_HC_rep1 WT_CC70_H3K27ac_HC
- GSM8783830 WT_CC70_H3K27ac_HC_rep2 WT_CC70_H3K27ac_HC
- GSM8783831 WT_CC70_H3K27me3_HC_rep1 WT_CC70_H3K27me3_HC
- GSM8783832 WT_CC70_H3K27me3_HC_rep2 WT_CC70_H3K27me3_HC
- GSM8783833 WT_CC70_H3K4me3_HC_rep1 WT_CC70_H3K4me3_HC
- GSM8783834 WT_CC70_H3K4me3_HC_rep2 WT_CC70_H3K4me3_HC
- GSM8783835 WT_CnC10_H3K27ac_HC_rep1 WT_CnC10_H3K27ac_HC
- GSM8783836 WT_CnC10_H3K27ac_HC_rep2 WT_CnC10_H3K27ac_HC
- GSM8783837 WT_CnC10_H3K27me3_HC_rep1 WT_CnC10_H3K27me3_HC
- GSM8783838 WT_CnC10_H3K27me3_HC_rep2 WT_CnC10_H3K27me3_HC
- GSM8783839 WT_CnC10_H3K4me3_HC_rep1 WT_CnC10_H3K4me3_HC
- GSM8783840 WT_CnC10_H3K4me3_HC_rep2 WT_CnC10_H3K4me3_HC
- GSM8783841 WT_CC10_H3K27ac_BS_rep1 WT_CC10_H3K27ac_BS
- GSM8783842 WT_CC10_H3K27ac_BS_rep2 WT_CC10_H3K27ac_BS
- GSM8783843 WT_CC10_H3K27me3_BS_rep1 WT_CC10_H3K27me3_BS
- GSM8783844 WT_CC10_H3K27me3_BS_rep2 WT_CC10_H3K27me3_BS
- GSM8783845 WT_CC10_H3K4me3_BS_rep1 WT_CC10_H3K4me3_BS
- GSM8783846 WT_CC10_H3K4me3_BS_rep2 WT_CC10_H3K4me3_BS
- GSM8783847 WT_CC30_H3K27ac_BS_rep1 WT_CC30_H3K27ac_BS
- GSM8783848 WT_CC30_H3K27ac_BS_rep2 WT_CC30_H3K27ac_BS
- GSM8783849 WT_CC30_H3K27me3_BS_rep1 WT_CC30_H3K27me3_BS
- GSM8783850 WT_CC30_H3K27me3_BS_rep2 WT_CC30_H3K27me3_BS
- GSM8783851 WT_CC30_H3K4me3_BS_rep1 WT_CC30_H3K4me3_BS
- GSM8783852 WT_CC30_H3K4me3_BS_rep2 WT_CC30_H3K4me3_BS
- GSM8783853 WT_CnC10_H3K27ac_BS_rep1 WT_CnC10_H3K27ac_BS
- GSM8783854 WT_CnC10_H3K27ac_BS_rep2 WT_CnC10_H3K27ac_BS
- GSM8783855 WT_CnC10_H3K27me3_BS_rep1 WT_CnC10_H3K27me3_BS
- GSM8783856 WT_CnC10_H3K27me3_BS_rep2 WT_CnC10_H3K27me3_BS
+ 17 more — browse all 57 samples with per-sample file links →
- GSE275917 Nup153 regulates neuronal responsiveness through HDAC1-mediated epigenetic modulation [ChIP-seq] 17 samples shares epigenetic, chip-seq
- GSE299381 KAT6A Chimeras Forms a Self-Reinforcing Epigenetic Module with NURF and MLL/COMPASS in AML [ChIP-Seq] 13 samples shares epigenetic, chip-seq
- GSE207943 Epigenetic plasticity cooperates with emergent cell-cell interactions to drive neoplastic tissue remodeling in the pancreas 59 samples shares epigenetic, remodeling
- GSE327565 Sustained Yap/Taz activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling 14 samples shares persistent, remodeling
- GSE326112 Interleukin-12 drives a rapid STAT4/DDX5-dependent change in the RNA polymerase II landscape for IFN-γ production by NK cells [CUT&RUN] 18 samples shares ifn
- GSE237643 Deletion of the mRNA endonuclease Regnase-1 promotes NK cell anti-tumor activity via OCT2- dependent transcription of Ifng 58 samples shares ifn
- GSE300933 Ptpn2 limits plasma cell fate and antiviral immunity by integrating B cell receptor and IFN-γ signals in B cells 23 samples shares ifn
- GSE324935 IFN-γ and TLR9 signaling reprogram tumor-associated macrophages to promote antitumor immunity in melanoma 20 samples shares ifn
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.