This study explores how YAP/TAZ-TEAD signaling regulates endothelial cell metabolism and angiogenesis. Endothelial-specific deletion of YAP/TAZ reduced nutrient transporter expression and mTORC1 activity, impairing proliferation. A constitutively active TAZ mutant (TAZ^S89A), expressed from the Rosa26 locus, restored angiogenic capacity.
YAP/TAZ-TEAD promotes endothelial nutrient uptake and mTORC1 signaling, driving angiogenesis; disruption impairs vascular growth, highlighting a therapeutic axis.
Rosa26 Knockin mouse expressing constitutively active TAZ^S89A under endothelial-specific Cre control, using IRES technology for bicistronic expression of a reporter.
Angiogenesis, Endothelial metabolism, mTORC1, YAP/TAZ pathway, Nutrient sensing
Rosa26 Knockin, IRES-reporter, TAZ^S89A mutant, Conditional Cre-lox system
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
