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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Defective angiogenesis in mice lacking endoglin.

Endoglin is a transforming growth factor-beta ( TGF-beta) binding protein expressed on the surface of endothelial cells. Loss-of-function mutations in the human endoglin gene ENG cause hereditary hemorrhagic telangiectasia (HHT1), a disease characterized by vascular malformations. Here it is shown that by gestational day 11.5, mice lacking endoglin die from defective vascular development. However, in contrast to mice lacking TGF-beta, vasculogenesis was unaffected. Loss of endoglin caused poor vascular smooth muscle development and arrested endothelial remodeling. These results demonstrate that endoglin is essential for angiogenesis and suggest a pathogenic mechanism for HHT1.[1]

References

  1. Defective angiogenesis in mice lacking endoglin. Li, D.Y., Sorensen, L.K., Brooke, B.S., Urness, L.D., Davis, E.C., Taylor, D.G., Boak, B.B., Wendel, D.P. Science (1999) [Pubmed]
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