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HMGN3 ChIP-seq in AC16 cells and Bulk-RNAseq in AC16 cell with and without HMGN3 knockdown

GSE306626 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2025/12/02 Platform GPL34284
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 12 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
12 samples: 3 × AC16 cell, wildtype, BulkRNA-seq, vs 3 × AC16 cell, HMGN3 knockdown, BulkRNA-seq, vs 3 × AC16 cell, wildtype, ChIP-seq, vs 3 × AC16 cell, HMGN3 knockdown, ChIP-seq,Groups 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
Chromatin structural gene expression stratifies cardiac cell populations in health and diseaseEpigenetics · 2025
Summary (written by the submitters)
Chromatin structure plays a central role in regulating gene expression and maintaining cellular identity, yet the structural factors driving these processes in cardiac disease remain poorly defined. To investigate whether these factors can distinguish healthy from diseased cardiac cell populations, we generated a comprehensive list of chromatin structural genes based on an extensive literature review.
Read the full summary ↓
Applying this list to a published single-cell RNA sequencing (scRNA-seq) dataset from human hearts with and without dilated cardiomyopathy (DCM), we found that chromatin structural gene expression effectively stratified cardiomyocyte and fibroblast populations by disease status. Diseased cardiomyocytes exhibited reduced expression of contractile genes and increased expression of cardiomyopathy markers, while fibroblasts showed enhanced activation signatures. Among these factors, HMGN3 emerged as a candidate of interest, showing consistent downregulation in cardiomyocytes from human patients, as well as in mouse (pressure overload) and pig (myocardial infarction) models of heart failure. Functional studies in AC16 cells revealed that HMGN3 depletion reduced proliferation, increased apoptosis, and decreased active chromatin marks (H3K27ac, H3K4me1), accompanied by increased chromatin compaction. These findings identify HMGN3 as a potential regulator of chromatin architecture in diseased cardiomyocytes, highlight the utility of chromatin structural gene expression in distinguishing pathological cardiac states, and reinforce the role of chromatin organization in shaping the cardiac phenotype. In this dataset, HMGN3 ChIP-seq and Bulk-RNAseq data with and without HMGN3 knockdown were generated using AC16 cells.
Published in
Chromatin structural gene expression stratifies cardiac cell populations in health and disease
Geng X, Pradeep R, Porter R et al. · Epigenetics 2025 · PMID 41117190 · doi:10.1080/15592294.2025.2566505
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 GSE306626_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1311517 and SRA study SRP613704. Searching any of these in the dataset finder brings you back here.

Study design
3 × AC16 cell, wildtype, BulkRNA-seq, vs 3 × AC16 cell, HMGN3 knockdown, BulkRNA-seq, vs 3 × AC16 cell, wildtype, ChIP-seq, vs 3 × AC16 cell, HMGN3 knockdown, ChIP-seq,

Supports a case/control comparison: 6 samples read as cases, 6 as controls.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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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