Format

Send to

Choose Destination
EMBO Rep. 2001 May;2(5):438-45.

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

Author information

1
Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.

Abstract

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.

PMID:
11375937
PMCID:
PMC1083887
DOI:
10.1093/embo-reports/kve093
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for HighWire Icon for PubMed Central
Loading ...
Support Center