Regions outside the major receptor binding interface of DLL1 and DLL4 contribute to context-dependent divergence of ligand function in vivo and differential Notch1 and Notch2 activation in vitro.

The multiple PDZ domain protein recruits Notch ligands to Nectin-2, which increases Notch signaling activity during angiogenesis.

Fringe proteins regulate Notch pathway differentially in the stem cell zone and progenitor compartment of the mouse intestinal epithelium to promote homeostasis.

Notch ligands from the Delta and Jagged families have distinct roles in epithelial progenitor cell fate of extrapulmonary and intrapulmonary airways and differentially restrict expansion of the neuroendocrine microenvironment.

MLL4 (KMT2D) is a major mammalian H3K4 mono- and di-methyltransferase that is essential for enhancer activation, cell-type-specific gene expression, and cell differentiation.

Notch ligand, Dll4 needs the flexible loop structure in the MNNL domain of the extracellular region to efficiently trigger the Notch signaling.

Notch ligands Jag1 and Dll4 and their effector Ephb2 are required in sinus venosus endocardium for primitive coronary vasculature formation and later for arterial differentiation and maturation of coronary endothelium.

The transfer of O-GlcNAc by EOGT to specific EGF repeats of NOTCH1 promotes DLL4 binding, Notch signaling, and retinal vascular development.

Increasing levels of the growth factor Vegfa disrupt blood vessel branching morphogenesis and drive diameter increase by synchronizing Notch signalling fluctuations between endothelial cells.

Bone formation in adult mice can be induced by a bone-binding, recombinant version of the Notch ligand Delta-like 4 without triggering adverse effects in other organs.