Rescue of the early vascular defects in Tek/Tie2 null mice reveals an essential survival function
AUTOR(ES)
Jones, Nina
FONTE
Oxford University Press
RESUMO
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 tekΔsp 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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1083887Documentos Relacionados
- Bub3 gene disruption in mice reveals essential mitotic spindle checkpoint function during early embryogenesis
- A Unique Autophosphorylation Site on Tie2/Tek Mediates Dok-R Phosphotyrosine Binding Domain Binding and Function
- Erk5 null mice display multiple extraembryonic vascular and embryonic cardiovascular defects
- Tie-1 and tie-2 define another class of putative receptor tyrosine kinase genes expressed in early embryonic vascular system.
- Genetic Analysis of Sorting Nexins 1 and 2 Reveals a Redundant and Essential Function in Mice