Antonio Duarte

TL;DR: Dll4 is revealed as a negative regulator of vascular sprouting and vessel branching that is required for normal vascular network formation during development by inhibiting endothelial tip cell formation.

TL;DR: It is demonstrated that VEGFR-3 is highly expressed in angiogenic sprouts, and genetic targeting or blocking of VEG FR-3 signalling with monoclonal antibodies results in decreased sprouting, vascular density, vessel branching and endothelial cell proliferation in mouse angiogenesis models, implicate VEGfr-3 as a regulator of vascular network formation.

TL;DR: It is shown that the Dll4 ligand alone is required in a dosage-sensitive manner for normal arterial patterning in development, which implicates Dll 4 as the specific mammalian endothelial ligand for autocrine endothelial Notch signaling, and suggests that Dll3 may be a suitable target for intervention in arterial angiogenesis.

TL;DR: It is demonstrated that DL4 is the essential and nonredundant N1 ligand responsible for T cell lineage commitment and strongly suggest that N1-expressing thymic progenitors interact with DL4- expressing TECs to suppress B lineage potential and to induce the first steps of intrathymic T cell development.

TL;DR: In this paper, a transcriptome analysis of retinal endothelial cells isolated from DLL4+/− and wild-type mice was performed to identify three clusters of tip cell-enriched genes encoding extracellular matrix degrading enzymes, basement membrane components and secreted molecules.