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DOT1L enhances BLM-induced pulmonary fibrosis by inducing endothelial-to-mesenchymal transition via H3K79me2 [ChIP-seq]

GSE297647 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 10 samples Submitted 2026/04/01 Platform GPL34284
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 10 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
10 samples: 3 × ChIP-H3K79me2-TGFβ vs 2 × ChIP-H3K79me2-ctrlGroups 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
DOT1L Drives Endothelial-to-Mesenchymal Transition and Fibrotic Vascular Remodeling via H3K79 MethylationAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
Summary (written by the submitters)
Endothelial-to-mesenchymal transition (EndoMT) have been reported to contribute to pulmonary fibrosis. Here, we showed that induction of EndoMT activated DOT1L expression and enhanced H3K79me2 level by TGFβ2 in human umbilical vein endothelial cells (HUVECs) in vitro. Using a bleomycin (BLM)-induced idiopathic pulmonary fibrosis (IPF) model, endothelial-lineage tracing reporter mice, and endothelial-specific Dot1L knockout mice, we confirmed that DOT1L mediates EndoMT and drives pulmonary fibrosis in vivo through H3K79 methylation.
Read the full summary ↓
ChIP-seq revealed direct binding of SMAD2/3 to the DOT1L promoter and increased H3K79me2 deposition at fibrosis-related genes following TGFβ2 stimulation.
Published in
DOT1L Drives Endothelial-to-Mesenchymal Transition and Fibrotic Vascular Remodeling via H3K79 Methylation
Wang Y, Peng X, Chen J et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2026 · PMID 41933932 · doi:10.1002/advs.202515581
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 GSE297647_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 PRJNA1265614 and SRA study SRP586769. Searching any of these in the dataset finder brings you back here.

Study design
3 × ChIP-H3K79me2-TGFβ vs 2 × ChIP-H3K79me2-ctrl

Supports a between-group comparison across 5 samples.

How we read this: 2 replicated groups read from 10 sample titles; they account for 5 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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