Helen M. Arthur

Endoglin expression in early development is associated with vasculogenesis and angiogenesis.

Mouse model for hereditary hemorrhagic telangiectasia has a generalized vascular abnormality.

Vascular endothelial growth factor induces abnormal microvasculature in the endoglin heterozygous mouse brain.

Endoglin promotes endothelial cell proliferation and TGF-beta/ALK1 signal transduction.

Defective paracrine signalling by TGFbeta in yolk sac vasculature of endoglin mutant mice: a paradigm for hereditary haemorrhagic telangiectasia.

A direct interaction between TGFbeta activated kinase 1 and the TGFbeta type II receptor: implications for TGFbeta signalling and cardiac hypertrophy.

Therapeutic levels of aspirin and salicylate directly inhibit a model of angiogenesis through a Cox-independent mechanism.

Endoglin has a crucial role in blood cell-mediated vascular repair.

Generation of a floxed allele of the mouse Endoglin gene.

Extracellular control of TGFbeta signalling in vascular development and disease.

Circulating endothelial progenitor cells exhibit diurnal variation.

Endoglin and activin receptor-like-kinase 1 are co-expressed in the distal vessels of the lung: implications for two familial vascular dysplasias, HHT and PAH.

Pathogenesis of arteriovenous malformations in the absence of endoglin.

Thalidomide stimulates vessel maturation and reduces epistaxis in individuals with hereditary hemorrhagic telangiectasia.

The TGFβ type II receptor plays a critical role in the endothelial cells during cardiac development.

The H9C2 cell line and primary neonatal cardiomyocyte cells show similar hypertrophic responses in vitro.

TGFβ signaling and congenital heart disease: Insights from mouse studies.

Angiotensin II-induced cardiomyocyte hypertrophy in vitro is TAK1-dependent and Smad2/3-independent.

Angiogenesis regulation by TGFβ signalling: clues from an inherited vascular disease.

Non-synonymous variants in the SMAD6 gene predispose to congenital cardiovascular malformation.

Minimal homozygous endothelial deletion of Eng with VEGF stimulation is sufficient to cause cerebrovascular dysplasia in the adult mouse.

Endothelial expression of TGFβ type II receptor is required to maintain vascular integrity during postnatal development of the central nervous system.

Deficiency for endoglin in tumor vasculature weakens the endothelial barrier to metastatic dissemination.

The tissue-specific RNA binding protein T-STAR controls regional splicing patterns of neurexin pre-mRNAs in the brain.