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Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice [RNA-seq Illumina]

GSE309117 Mus musculus (mouse) RNA-seq (gene expression) 18 samples Submitted 2025/11/13 Platform GPL34290
At a glance

RNA-seq (gene expression) · mouse · 18 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
18 samples: 6 conditions, mostly in triplicateGroups 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
Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in miceToxicological sciences : an official journal of the Society of Toxicology · 2026
Summary (written by the submitters)
Epidermal growth factor receptor (EGFR) is mostly known for its proliferative role in liver. Our earlier investigations indicated a paradoxical cell-death promoting facet of EGFR in acetaminophen (APAP)-induced liver injury (AILI) model. The current study investigates this unexpected role of EGFR in promoting AILI using a hepatocyte-specific EGFR deletion mouse model.
Read the full summary ↓
Hepatocyte-specific EGFR-deficient mice were generated by administering AAV8-TBG-CRE in EGFRfl/fl mice and were subsequently treated with a severely toxic dose (500 mg/kg) of APAP. Liver injury, regeneration and associated signaling pathways were assessed at different time intervals. EGFR deletion significantly attenuated the progression of liver injury (beyond 12hr post-APAP) without altering early liver injury (up to 6 hr) following APAP overdose. Consistently, the key injury initiating events such as APAP-protein adducts formation and early JNK activation remained intact in EGFR-deficient mice. However, EGFR deletion restricted prolonged JNK activation and its mitochondrial translocation, resulting in reduced propagation of mitochondrial damage and release of cell death drivers. Further, the replenishment of antioxidant glutathione (GSH), which is known to limit the progression of liver injury, was strikingly faster in EGFR-deficient mice. RNA-seq analysis and consequent validation revealed marked upregulation of autophagy and its transcriptional regulator TFEB, a key response to remove damaged mitochondria, in EGFR-deficient mice. Paradoxically, EGFR deletion also promoted compensatory liver proliferative response secondary to decreased progression of liver injury. Overall, hepatocyte-specific EGFR deletion halted the progression of AILI. Our study established an unexpected death promoting function of EGFR in AILI progression, which has wide implications in liver biology.
Published in
Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice
Jain S, Williams G, Mukherjee R et al. · Toxicological sciences : an official journal of the Society of Toxicology 2026 · PMID 41148051 · doi:10.1093/toxsci/kfaf151
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 GSE309117_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1333992 and SRA study SRP626418. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in triplicate
WT 0h ×3 KO 0h ×3 WT 6h ×3 KO 6h ×3 WT 24h ×3 KO 24h ×3

Supports a between-group comparison across 18 samples.

How we read this: 6 replicated groups read from 18 sample titles; they account for 18 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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