Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

KRAS mutation-induced EndMT of brain arteriovenous malformation is mediated through the TGF-β/BMP-SMAD4 pathway.

Stroke and vascular neurology - 1 Jun 2023

Xu Hongyuan, Huo Ran, Li Hao, Jiao Yuming, Weng Jiancong, Wang Jie, Yan Zihan, Zhang Junze, Zhao Shaozhi, He Qiheng, Sun Yingfan, Wang Shuo, Cao Yong

Abstract excerpt

OBJECTIVE: Somatic KRAS mutations have been identified in the majority of brain arteriovenous malformations (bAVMs), and subsequent in vivo experiments have confirmed that KRAS mutation in endothelial cells (ECs) causes AVMs in mouse and zebrafish models. Our previous study demonstrated that the KRASG12D mutant independently induced the endothelial-mesenchymal transition (EndMT), which was reversed by treatment...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Brain
Share to Human Umbilical Vein Endothelial Cells

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Intracranial Arteriovenous Malformations

Share to Proto-Oncogene Proteins p21(ras)

Share to Smad4 Protein

Share to Transforming Growth Factor beta

Share to Zebrafish

Source

Open in PubMed Open full text

Identifiers

PMID: 36418055
DOI: 10.1136/svn-2022-001700
PMCID: PMC10359780

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

KRAS mutation-induced EndMT of brain arteriovenous malformation is mediated through the TGF-β/BMP-SMAD4 pathway.PMID 36418055Read ↗

CRISPR/CasRx suppresses KRAS-induced brain arteriovenous malformation developed in postnatal brain endothelial cells in mice.Semantic proximity Read ↗

Advances in the Study of KRAS in Brain Arteriovenous Malformation.Semantic proximity Read ↗

Endothelial KRAS <sup>G12V</sup> signaling drives aberrant morphogenesis and establishes an AVM transcriptional identity in primary human endothelial cellsSemantic proximity Read ↗

Somatic Gain of KRAS Function in the Endothelium Is Sufficient to Cause Vascular Malformations That Require MEK but Not PI3K Signaling.Semantic proximity Read ↗

Somatic Activating KRAS Mutations in Arteriovenous Malformations of the Brain.Semantic proximity Read ↗

Review of treatment and therapeutic targets in brain arteriovenous malformation.Semantic proximity Read ↗

Exosomal miR-3131 derived from endothelial cells with KRAS mutation promotes EndMT by targeting PICK1 in brain arteriovenous malformations.Semantic proximity Read ↗

Evidence for endothelial‐to‐mesenchymal transition in human brain arteriovenous malformationsSemantic proximity Read ↗

Advances in the Genetics and Molecular Biology of Brain Arteriovenous Malformations.Semantic proximity Read ↗

Mutant KRAS in brain endothelial cells promotes vascular inflammation and impairs vascular integrity in brain arteriovenous malformation.Semantic proximity Read ↗

KLF4 is a key determinant in the development and progression of cerebral cavernous malformations.Semantic proximity Read ↗

MEK signaling represents a viable therapeutic vulnerability of <i>KRAS</i> -driven somatic brain arteriovenous malformationsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.