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Article

Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling.

Nature cell biology - 1 Jun 2017

Jin Yi, Muhl Lars, Burmakin Mikhail, Wang Yixin, Duchez Anne-Claire, Betsholtz Christer, Arthur Helen M, Jakobsson Lars

Abstract excerpt

Loss-of-function (LOF) mutations in the endothelial cell (EC)-enriched gene endoglin (ENG) cause the human disease hereditary haemorrhagic telangiectasia-1, characterized by vascular malformations promoted by vascular endothelial growth factor A (VEGFA). How ENG deficiency alters EC behaviour to trigger these anomalies is not understood. Mosaic ENG deletion in the postnatal mouse rendered Eng LOF ECs insensitive...

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Share to Arteriovenous Malformations
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Neovascularization, Physiologic

Share to Phosphatidylinositol 3-Kinase

Share to Stress, Mechanical

Share to Telangiectasia, Hereditary Hemorrhagic

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Share to Vascular Endothelial Growth Factor Receptor-2

Source

Open in PubMed Open full text

Identifiers

PMID: 28530660
DOI: 10.1038/ncb3534
PMCID: PMC5467724

Genes

ENG
VEGFA

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

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Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling.PMID 28530660Read ↗

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