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

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

CNS neuroscience & therapeutics - 1 May 2023

He Qiheng, Huo Ran, Wang Jie, Xu Hongyuan, Zhao Shaozhi, Zhang Junze, Sun Yingfan, Jiao Yuming, Weng Jiancong, Zhao Jizong, Cao Yong

Abstract excerpt

AIMS: To explore the underlying mechanism by which low-frequency KRAS mutations result in extensive EndMT occurrence. METHODS: Exosomes derived from primarily cultured brain arteriovenous malformation (bAVMs) and human umbilical vein endothelial cells (HUVECs) transfected with KRASG12D , KRASWT , or KRASNC lentiviruses were isolated, and their effects on HUVECs were identified by western blotting and...

Read the complete abstract on PubMed

Topics

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

Share to Brain
Share to Carrier Proteins

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

Share to Human Umbilical Vein Endothelial Cells

Share to Intracranial Arteriovenous Malformations

Share to MicroRNAs

Share to Mutation

Share to Nuclear Proteins

Share to Proto-Oncogene Proteins p21(ras)

Source

Open in PubMed Open full text

Identifiers

PMID: 36718590
DOI: 10.1111/cns.14103
PMCID: PMC10068464

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

Exosomal miR-3131 derived from endothelial cells with KRAS mutation promotes EndMT by targeting PICK1 in brain arteriovenous malformations.PMID 36718590Read ↗

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

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

De Novo Germline and Somatic Variants Convergently Promote Endothelial-to-Mesenchymal Transition in Simplex Brain Arteriovenous MalformationSemantic proximity Read ↗

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

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

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

Development and characterization of a human model of arteriovenous malformation (AVM)-on-a-chipSemantic proximity Read ↗

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

Targeting miR-9 in Glioma Stem Cell-Derived Extracellular Vesicles: A Novel Diagnostic and Therapeutic BiomarkerSemantic proximity Read ↗

Endothelial oncogenic KRAS mutation drives the dynamics of microglia and macrophages in brain arteriovenous malformation.Semantic proximity Read ↗

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

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