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KANSL3 directs transcriptional programs essential for hepatic metabolism and differentiation [scRNA-seq]

GSE277833 Mus musculus (mouse) Single-cell RNA-seq 12 samples Submitted 2025/09/23 Platform GPL24247
At a glance

Single-cell RNA-seq · mouse · 12 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart.
Organism
Mus musculus (mouse)
Samples
12 samples: 4 × scRNAseq, neonatal liver, WT, vs 4 × scRNAseq, neonatal liver, Kansl3 LKO, vs 2 × scRNAseq, old liver, Kansl3 LKO, vs 2 × scRNAseq, old liver, WT,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
KANSL3 directs transcriptional programs essential for hepatic metabolism and differentiationLife science alliance · 2025
Summary (written by the submitters)
Understanding the molecular mechanisms governing liver homeostasis and disease progression is crucial for developing new therapeutic strategies for chronic liver diseases and liver cancer, with emerging evidence underscoring the key role of epigenetic regulation. Here, we show that hepatic deletion of the epigenetic regulator KANSL3, a component of the NSL complex, causes early-onset chronic liver disease, distinct from metabolic dysfunction-associated steatohepatitis (MASH).
Read the full summary ↓
Loss of KANSL3 leads to biliary hyperplasia and early hepatic fibrosis, indicating its vital role in liver structure and function. KANSL3 acts as a master regulator of hepatocyte gene expression through histone acetylation, impacting global liver transcriptional networks. scRNA-seq analysis uncovers that KANSL3 deletion disrupts hepatocyte differentiation in vivo and in hepatic organoids. Ultimately, chronic KANSL3 loss alters the liver microenvironment and promotes an immunosuppressive premalignant state linked to hepatocellular carcinoma (HCC).
Published in
KANSL3 directs transcriptional programs essential for hepatic metabolism and differentiation
Wiese M, Pessoa Rodrigues C, Akbas ME et al. · Life science alliance 2025 · PMID 41044006 · doi:10.26508/lsa.202503238
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 GSE277833_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1164293 and SRA study SRP534257. Searching any of these in the dataset finder brings you back here.

Study design
4 × scRNAseq, neonatal liver, WT, vs 4 × scRNAseq, neonatal liver, Kansl3 LKO, vs 2 × scRNAseq, old liver, Kansl3 LKO, vs 2 × scRNAseq, old liver, WT,

Supports a between-group comparison across 12 samples.

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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