<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">van Laake, Linda W</style></author><author><style face="normal" font="default" size="100%">van den Driesche, Sander</style></author><author><style face="normal" font="default" size="100%">Post, Simone</style></author><author><style face="normal" font="default" size="100%">Feijen, Alie</style></author><author><style face="normal" font="default" size="100%">Jansen, Maurits A</style></author><author><style face="normal" font="default" size="100%">Driessens, Mariette H</style></author><author><style face="normal" font="default" size="100%">Mager, Johannes J</style></author><author><style face="normal" font="default" size="100%">Snijder, Repke J</style></author><author><style face="normal" font="default" size="100%">Westermann, Cornelius J J</style></author><author><style face="normal" font="default" size="100%">Doevendans, Pieter A</style></author><author><style face="normal" font="default" size="100%">Van Echteld, Cees J A</style></author><author><style face="normal" font="default" size="100%">ten Dijke, Peter</style></author><author><style face="normal" font="default" size="100%">Arthur, Helen M</style></author><author><style face="normal" font="default" size="100%">Goumans, Marie-José</style></author><author><style face="normal" font="default" size="100%">Lebrin, Franck</style></author><author><style face="normal" font="default" size="100%">Mummery, Christine L</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Endoglin has a crucial role in blood cell-mediated vascular repair.</style></title><secondary-title><style face="normal" font="default" size="100%">Circulation</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Circulation</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Antigens, CD</style></keyword><keyword><style  face="normal" font="default" size="100%">Cells, Cultured</style></keyword><keyword><style  face="normal" font="default" size="100%">Coronary Vessels</style></keyword><keyword><style  face="normal" font="default" size="100%">Heterozygote</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Ligation</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Monocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Myocardial Infarction</style></keyword><keyword><style  face="normal" font="default" size="100%">Myocardium</style></keyword><keyword><style  face="normal" font="default" size="100%">Neovascularization, Physiologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Cell Surface</style></keyword><keyword><style  face="normal" font="default" size="100%">Telangiectasia, Hereditary Hemorrhagic</style></keyword><keyword><style  face="normal" font="default" size="100%">Ventricular Remodeling</style></keyword><keyword><style  face="normal" font="default" size="100%">Wound Healing</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2006 Nov 21</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">114</style></volume><pages><style face="normal" font="default" size="100%">2288-97</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Endoglin, an accessory receptor for transforming growth factor-beta in vascular endothelial cells, is essential for angiogenesis during mouse development. Mutations in the human gene cause hereditary hemorrhagic telangiectasia type 1 (HHT1), a disease characterized by vascular malformations that increase with age. Although haploinsufficiency is the underlying cause of the disease, HHT1 individuals show great heterogeneity in age of onset, clinical manifestations, and severity.</style></abstract><issue><style face="normal" font="default" size="100%">21</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/17088457?dopt=Abstract</style></custom1></record></records></xml>