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Article

Endoglin is required in Pax3-derived cells for embryonic blood vessel formation.

Developmental biology - 1 Jan 2016

Young K, Krebs L T, Tweedie E, Conley B, Mancini M, Arthur H M, Liaw L, Gridley T, Vary Cph

Abstract excerpt

Mutations in endoglin, a TGFβ/BMP coreceptor, are causal for hereditary hemorrhagic telangiectasia (HHT). Endoglin-null (Eng-/-) mouse embryos die at embryonic day (E)10.5-11.5 due to defects in angiogenesis. In part, this is due to an absence of vascular smooth muscle cell differentiation and vessel investment. Prior studies from our lab and others have shown the importance of endoglin expression in embryonic...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 26481065
DOI: 10.1016/j.ydbio.2015.10.019
PMCID: PMC4688190

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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Endoglin is required in Pax3-derived cells for embryonic blood vessel formation.PMID 26481065Read ↗

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