H3K4me3 instructs transcription at intergenic active regulatory elements [ChIP-seq]
ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 35 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
- Homo sapiens (human)
- Samples
- 35 samples: 14 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
- H3K4me3 amplifies transcription at intergenic active regulatory elementsGenes & development · 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 GSE290054_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 PRJNA1226113 and SRA study SRP565237. Searching any of these in the dataset finder brings you back here.
Supports a between-group comparison across 28 samples.
How we read this: 14 replicated groups read from 35 sample titles; they account for 28 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.
- GSM8804769 H3K4me1_WT_rep1 H3K4me1_WT
- GSM8804770 H3K4me1_WT_rep2 H3K4me1_WT
- GSM8804771 H3K4me1_PRDM9_rep1 H3K4me1_PRDM9
- GSM8804772 H3K4me1_PRDM9_rep2 H3K4me1_PRDM9
- GSM8804773 H3K4me1_cdPRDM9_rep1 H3K4me1_cdPRDM9
- GSM8804774 H3K4me1_cdPRDM9_rep2 H3K4me1_cdPRDM9
- GSM8804775 H3K4me2_WT_rep1 H3K4me2_WT
- GSM8804776 H3K4me2_WT_rep2 H3K4me2_WT
- GSM8804777 H3K4me3_WT_rep1 H3K4me3_WT
- GSM8804778 H3K4me3_WT_rep2 H3K4me3_WT
- GSM8804779 H3K4me3_PRDM9_rep1 H3K4me3_PRDM9
- GSM8804780 H3K4me3_PRDM9_rep2 H3K4me3_PRDM9
- GSM8804781 H3K4me3_cdPRDM9_rep1 H3K4me3_cdPRDM9
- GSM8804782 H3K4me3_cdPRDM9_rep2 H3K4me3_cdPRDM9
- GSM8804783 H3K4me3_acCREs
- GSM8804784 H3K4me3_PEs
- GSM8804785 H3K4me3_UOs
- GSM8804786 H3K4me3_mFOXQ1
- GSM8804787 H3K4me3_mSOX9
- GSM8804788 H3K27ac_WT_rep1 H3K27ac_WT
- GSM8804789 H3K27ac_WT_rep2 H3K27ac_WT
- GSM8804790 H3K27ac_PRDM9_rep1 H3K27ac_PRDM9
- GSM8804791 H3K27ac_PRDM9_rep2 H3K27ac_PRDM9
- GSM8804792 H3K27ac_cdPRDM9_rep1 H3K27ac_cdPRDM9
- GSM8804793 H3K27ac_cdPRDM9_rep2 H3K27ac_cdPRDM9
- GSM8804794 Pol2_WT_rep1 Pol2_WT
- GSM8804795 Pol2_WT_rep2 Pol2_WT
- GSM8804796 Pol2-S5P_WT_rep1 Pol2-S5P_WT
- GSM8804797 Pol2-S5P_WT_rep2 Pol2-S5P_WT
- GSM8804798 Pol2-S5P_PRDM9_rep1 Pol2-S5P_PRDM9
- GSM8804799 Pol2-S5P_PRDM9_rep2 Pol2-S5P_PRDM9
- GSM8804800 Pol2-S5P_cdPRDM9_rep1 Pol2-S5P_cdPRDM9
- GSM8804801 Pol2-S5P_cdPRDM9_rep2 Pol2-S5P_cdPRDM9
- GSM8804802 input_PRDM9
- GSM8804803 input_cdPRDM9
- GSE302930 Epigenetic Atlas of Bladder Cancer Reveals Master Transcription Factors and Risk-Associated Regulatory Elements in Luminal and Basal-Squamous Molecular Subtypes 92 samples shares transcription, regulatory, elements
- GSE280574 mChIP-seq for high-throughput epigenomic profiling reveals a decoupling of H2A.Z and H3K4me3 in cancer 576 samples shares h3k4me3, chip-seq
- GSE284519 TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination [ChIP-seq] 93 samples shares transcription, chip-seq
- GSE296190 Hypoxic regulation of chromatin and gene transcription [ChIP-seq] 84 samples shares transcription, chip-seq
- GSE335058 Evolutionary guided transcription factor design programs novel T cell states [ChIP-Seq] 66 samples shares transcription, chip-seq
- GSE293334 Allelic topological centering by transcription factors drives oncogenic multi-enhancer transcriptional regulation [ChIP-seq] 60 samples shares transcription, chip-seq
- GSE296831 Epigenetic Context Defines the Transcriptional Activity of Canonical and Noncanonical NF-kappaB Signaling in Pancreatic Cancer [ChIP-Seq] 48 samples shares transcription, chip-seq
- GSE259248 ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer (ChIP-Seq) 36 samples shares transcription, chip-seq
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.