GEO series

Nrf2-mediated chromatin activation of hyperosmotic response genes attenuates heat-induced renal injury [ChIP-seq]

GSE266022 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 24 samples Submitted 2026/07/29 Platform GPL24247

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 24 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: 24 samples: 24 samples, each with a distinct title — no replicated groupsGroups 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: Nrf2-mediated epigenetic priming of osmoprotective genes enhances cellular adaptation to hyperosmotic stressThe Journal of biological chemistry · 2026

Summary (written by the submitters)

The escalating frequency and duration of extreme weather events, driven by ongoing climate change, are heightening health hazards associated with heat stress. Heat stress can cause whole-body hyperosmolarity and increase risk of chronic kidney disease. Here, we confirmed Nrf2 as the core transcription factor for cellular resistance to hyperosmotic stress through drug screening.

Read the full summary ↓

Meanwhile, we constructed a mouse model of renal injury caused by high temperature dehydration, genetic deletion of Nrf2 further increased the renal injury and fibrosis. The natural compound SFN, found in cruciferous plants, can be used to activate Nrf2 and alleviate kidney damage caused by high-temperature dehydration. Mechanistically, we performed hyperosmotic stress in kidney collecting duct cells, and through ATAC-seq and ChIP-seq analysis of multiple histone modifications, found that most of the hyperosmotic response genes changed their chromatin state after pharmacological activation of Nrf2. The activation of the chromatin state in hyperosmotic response genes enhances the binding affinity of Nfat5 following exposure to hyperosmotic stress. Together, activation of Nrf2 maintains the active chromatin state of hyperosmotic response genes. Under hyperosmotic stress, the core transcription factor Nfat5 efficiently activates gene expression, thereby assisting cells in resisting hyperosmotic stress. Additionally, activation of Nrf2 by SFN may serve as a potential therapeutic approach for preventing renal injury caused by high-temperature dehydration.

Published in

Nrf2-mediated epigenetic priming of osmoprotective genes enhances cellular adaptation to hyperosmotic stress

Lu Y, Li N, Dou X et al. · The Journal of biological chemistry 2026 · PMID 42331111 · doi:10.1016/j.jbc.2026.113278

This dataset

Open GSE266022 in finder → Find more mouse ChIP / ATAC / CUT&Tag datasets →

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.

Series matrix ↓

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 GSE266022_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

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.

Raw reads on ENA ↗

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 PRJNA1105358 and SRA study SRP504398. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42331111) ↗

Study design

24 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 24 sample titles: 24 distinct titles with little repetition. 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

GSM8239588 mIMCD3 cells, Input-DMSO
GSM8239589 mIMCD3 cells, Input-SFN
GSM8239590 mIMCD3 cells, K27ac-DMSO
GSM8239591 mIMCD3 cells, K27ac-SFN
GSM8239592 mIMCD3 cells, K27me3_DMSO
GSM8239593 mIMCD3 cells, K27me3_SFN
GSM8239594 mIMCD3 cells, K36me3_DMSO
GSM8239595 mIMCD3 cells, K36me3_SFN
GSM8239596 mIMCD3 cells, K4me1_DMSO
GSM8239597 mIMCD3 cells, K4me1_SFN
GSM8239598 mIMCD3 cells, K4me3_DMSO
GSM8239599 mIMCD3 cells, K4me3_SFN
GSM8239600 mIMCD3 cells, K9ac-DMSO
GSM8239601 mIMCD3 cells, K9ac-SFN
GSM8239602 mIMCD3 cells, K9me3_DMSO
GSM8239603 mIMCD3 cells, K9me3_SFN
GSM8239605 mIMCD3 cells, NFAT5-ChIP-HS-1h-SFN
GSM8239606 mIMCD3 cells, NFAT5-DMSO
GSM8239607 mIMCD3 cells, NFAT5-DMSO-1h
GSM8239608 mIMCD3 cells, NFAT5-SFN
GSM8239610 mIMCD3 cells, Nrf2_DMSO
GSM8239611 mIMCD3 cells, Nrf2_DMSO_HS1h
GSM8239613 mIMCD3 cells, Nrf2_SFN
GSM8239614 mIMCD3 cells, Nrf2_SFN_HS1h

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GSE232327 Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury 41 samples shares activation, injury
GSE333586 Formylpeptide Receptor Activation Attenuates Renovascular Remodeling in Neurogenic Hypertension (Left Ventricle) 26 samples shares activation, attenuates
GSE333587 Formylpeptide Receptor Activation Attenuates Renovascular Remodeling in Neurogenic Hypertension (Kidney) 19 samples shares activation, attenuates

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