← BioTransfer GEO Dataset Finder
GEO series

KRAS-Dependent Metabolic Reprogramming of Endothelial Cells as a Therapeutic Vulnerability in Brain Arteriovenous Malformations

GSE292538 Homo sapiens (human) RNA-seq (gene expression) 18 samples Submitted 2025/12/15 Platform GPL34284
At a glance

RNA-seq (gene expression) · human · 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
Homo sapiens (human)
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
KRAS-dependent glycolytic reprogramming of endothelial cells in sporadic arteriovenous malformationsEMBO molecular medicine · 2026
Summary (written by the submitters)
Brain arteriovenous malformation (bAVM) is a disease characterized by the formation of tangled blood vessels with direct connections between arteries and veins. There is currently limited understanding of the underlying molecular mechanisms that are responsible for the development of bAVM. Our previous work identified the presence of somatic activating KRAS mutations in endothelial cells (ECs) isolated from clinical bAVM tissue.
Read the full summary ↓
Given the association between mutant KRAS, metabolic reprogramming and EC angiogenesis, we aimed to investigate if altered endothelial metabolism is involved in the pathogenesis of bAVM to drive abnormal vascular remodeling. As such, we engineered a human EC model with inducible expression of mutant KRAS G12V. We observed a significant increase in glucose metabolism upon mutant KRAS expression. This elevation in EC glycolysis contributes to the angiogenic behaviours that are observed in our mutant KRAS EC models. To further explore the transcriptional alterations underlying these changes, we performed this RNA-sequencing study with various glycolysis inhibitors and a MEK inhibitor (the major signaling pathway altered in mutant KRAS ECs) to profile the impact of glucose metabolism changes on endothelial biology.
Published in
KRAS-dependent glycolytic reprogramming of endothelial cells in sporadic arteriovenous malformations
Wu R, Khosraviani N, Mansur A et al. · EMBO molecular medicine 2026 · PMID 41708990 · doi:10.1038/s44321-026-00383-y
This dataset
Open GSE292538 in finder → Find more human RNA-seq 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 GSE292538_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: 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 PRJNA1240093 and SRA study SRP572128. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41708990) ↗
Study design
6 conditions, mostly in triplicate
Telo-HUVECs, KRAS G12V, no doxycycline, no tr… ×3 Telo-HUVECs, KRAS G12V, doxycycline induction… ×3 Telo-HUVECs, KRAS G12V, doxycycline induction… ×3 Telo-HUVECs, KRAS G12V, doxycycline induction… ×3 Telo-HUVECs, KRAS G12V, doxycycline induction… ×3 Telo-HUVECs, KRAS G12V, doxycycline induction… ×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
Datasets on a similar topic

Search all human RNA-seq datasets in GEO →

Share this dataset

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.