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Publication : Rescue of the early vascular defects in Tek/Tie2 null mice reveals an essential survival function.

First Author  Jones N Year  2001
Journal  EMBO Rep Volume  2
Issue  5 Pages  438-45
PubMed ID  11375937 Mgi Jnum  J:115217
Mgi Id  MGI:3691072 Doi  10.1093/embo-reports/kve093
Citation  Jones N, et al. (2001) Rescue of the early vascular defects in Tek/Tie2 null mice reveals an essential survival function. EMBO Rep 2(5):438-45
abstractText  Disruption of the signaling pathways mediated by the receptor tyrosine kinase Tek/Tie2 has shown that this receptor plays a pivotal role in vascularization of the developing embryo. In this report, we have utilized the tetracycline-responsive binary transgenic system to overcome the early lethal cardiovascular defects associated with the tekDeltasp null allele in order to investigate the role of Tek in later stages of vessel growth. We show for the first time in vivo that synchronized loss of tek expression correlates with rapid endothelial cell apoptosis in hemorrhagic regions of the embryo, demonstrating an ongoing requirement for Tek-mediated signal transduction in vascular maintenance.
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