GEO series

Lactyl-HDAC1-Mediated Epigenetic Gating of Angiogenic Transcription via Metabolic Reprogramming [ChIP-seq]

GSE305252 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 2 samples Submitted 2025/11/04 Platform GPL24676

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 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: Homo sapiens (human)
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.

Summary (written by the submitters)

While angiogenesis serves as a cornerstone of embryogenesis and a defining feature of pathological progression, a critical gap persists in understanding how metabolic signaling precisely converges with nuclear reprogramming to ignite vascular growth. Here, we demonstrate that glucose-derived lactate via glycolysis induces site-specific lactylation at lysine 412 (K412) of histone deacetylase 1 (HDAC1), triggering transcriptional activation of pro-angiogenic genes such as VEGFA.

Read the full summary ↓

Mechanistically, HDAC2 forms a nuclear complex with HDAC1 to suppress its lactylation modification in the cytoplasm, whereas alanyl-tRNA synthetase (AARS1) promotes its lactylation in cytoplasm to prevent HDAC1 nuclear translocation, leading to nuclear accumulation of H3K56 acetylation and chromatin remodeling that selectively activates angiogenesis-related transcriptional programs. In zebrafish models, HDAC1-K412 mutation caused embryonic lethality, and site-specific lactylation dynamically increased during cardiac development. In the HDAC1 K412A mutation knock-in mouse model, the results showed that this site prevents vascular proliferation in the retinas of streptozotocin (STZ)-induced diabetic mice. Pharmacologically, we found that the HDAC1 activator Exifone suppressed its lactylation and inhibited vascular growth. Strikingly, Exifone attenuates pathological neovascularization in embryonic chick models and halts aberrant vascular proliferation within the retinal vasculature of STZ-diabetic mice. Our findings reveal HDAC1 lactylation as a metabolic-epigenetic nexus governing angiogenesis, providing mechanistic insights into not only obscures developmental principles but hampers therapeutic targeting of aberrant vascularization in diseases ranging from cancer to diabetes.

This dataset

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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 GSE305252_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 PRJNA1304921 and SRA study SRP608398. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 2 more — browse all 2 samples with per-sample file links →

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.