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Genetic and pharmaceutical manipulation of H3K9 methyltransferase Suv39h1 promotes liver regeneration by unleashing HMGB2 transcription

GSE313427 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 2 samples Submitted 2026/05/15 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 2 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
2 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
Genetic and pharmaceutical manipulation of H3K9 methyltransferase Suv39h1 promotes liver regeneration by unleashing HMGB2 transcriptionExperimental & molecular medicine · 2026
Summary (written by the submitters)
Robust liver regeneration counteracts and facilitates a recovery from liver injuries. The underlying epigenetic mechanisms, however, are not fully appreciated. In the present study we investigated the role of suppressor of variegation 3-9 homolog 1 (Suv39h1), a histone H3K9 methyltransferase, in liver regeneration. Suv39h1 expression was repressed by DNMT1 during liver regeneration.
Read the full summary ↓
Systemic or hepatocyte-specific deletion of Suv39h1 in mice enhanced liver regeneration and post-surgery survival following partial hepatectomy. RNA sequencing revealed high-mobility group protein B2 (HMGB2) as a target for Suv39h1. Suv39h1 down-regulation in proliferating hepatocytes allowed E2F1 to activate HMGB2 transcription. Consistently, HMGB2 knockdown attenuated proliferation of hepatocytes in response to HGF treatment and suppressed liver regeneration in mice. Integrated transcriptomic analysis indicated that HMGB2 might contribute to proliferation of hepatocytes by regulating a panel of pro-regenerative genes. Importantly, Suv39h1 inhibition by chaetocin boosted liver regeneration in mice. Finally, significant correlation between Suv39h1, HMGB2, and proliferative markers was identified in patients with acute liver failure. In conclusion, our data uncover an unrecognized role for Suv39h1 in liver regeneration. Therefore, targeting Suv39h1 may be considered as a viable strategy to boost liver regeneration after injury.
Published in
Genetic and pharmaceutical manipulation of H3K9 methyltransferase Suv39h1 promotes liver regeneration by unleashing HMGB2 transcription
Lu Y, Zhou J, Miao X et al. · Experimental & molecular medicine 2026 · PMID 41963467 · doi:10.1038/s12276-026-01677-4
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 GSE313427_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 PRJNA1379499 and SRA study SRP654393. Searching any of these in the dataset finder brings you back here.

Samples in this study

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