Endoglin

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  Subject Areas on Research

  • A phase I first-in-human study of TRC105 (Anti-Endoglin Antibody) in patients with advanced cancer. 
  • ALK5 phosphorylation of the endoglin cytoplasmic domain regulates Smad1/5/8 signaling and endothelial cell migration. 
  • Applicability of the Curaçao Criteria for the Diagnosis of Hereditary Hemorrhagic Telangiectasia in the Pediatric Population. 
  • Assignment of transforming growth factor beta1 and beta3 and a third new ligand to the type I receptor ALK-1. 
  • Clinical heterogeneity in hereditary haemorrhagic telangiectasia: are pulmonary arteriovenous malformations more common in families linked to endoglin? 
  • Endoglin deficiency impairs stroke recovery. 
  • Endoglin interacts with VEGFR2 to promote angiogenesis. 
  • Endoglin mediates fibronectin/α5β1 integrin and TGF-β pathway crosstalk in endothelial cells. 
  • Endoglin promotes transforming growth factor beta-mediated Smad 1/5/8 signaling and inhibits endothelial cell migration through its association with GIPC. 
  • Endoglin regulates PI3-kinase/Akt trafficking and signaling to alter endothelial capillary stability during angiogenesis. 
  • Endoglin, a TGF-beta binding protein of endothelial cells, is the gene for hereditary haemorrhagic telangiectasia type 1. 
  • Endoglin, an ancillary TGFbeta receptor, is required for extraembryonic angiogenesis and plays a key role in heart development. 
  • Expression analysis of endoglin missense and truncation mutations: insights into protein structure and disease mechanisms. 
  • Expression analysis of four endoglin missense mutations suggests that haploinsufficiency is the predominant mechanism for hereditary hemorrhagic telangiectasia type 1. 
  • Hereditary haemorrhagic telangiectasia: a questionnaire based study to delineate the different phenotypes caused by endoglin and ALK1 mutations. 
  • Modulation of circulating protein biomarkers following TRC105 (anti-endoglin antibody) treatment in patients with advanced cancer. 
  • Molecular classification of patients with unexplained hamartomatous and hyperplastic polyposis. 
  • Mutation and expression analysis of the endoglin gene in hereditary hemorrhagic telangiectasia reveals null alleles. 
  • Neonatal co-infection with helicobacter species markedly accelerates the development of inflammation-associated colonic neoplasia in IL-10(-/-) mice. 
  • Regulation of TGF-β receptor hetero-oligomerization and signaling by endoglin. 
  • SMAD4 mutations found in unselected HHT patients. 
  • Six novel mutations in the endoglin gene in hereditary hemorrhagic telangiectasia type 1 suggest a dominant-negative effect of receptor function. 
  • The interaction of endoglin with beta-arrestin2 regulates transforming growth factor-beta-mediated ERK activation and migration in endothelial cells. 
  • The modulation of MSC integrin expression by RGD presentation. 
  • The molecular genetics of hereditary hemorrhagic telangiectasia. 
  • Transcriptional profiling of human placentas from pregnancies complicated by preeclampsia reveals disregulation of sialic acid acetylesterase and immune signalling pathways. 
  • Transdifferentiation of human endothelial progenitors into smooth muscle cells. 
  • Two common endoglin mutations in families with hereditary hemorrhagic telangiectasia in the Netherlands Antilles: evidence for a founder effect. 
  • Vascular endothelial growth factor induces abnormal microvasculature in the endoglin heterozygous mouse brain. 
  • Vascular morphogenesis: tales of two syndromes.