Unbiased analyses highlight context-specific crosstalk between Notch, DNA damage response genes, and PP2A, and provide a roadmap for understanding how Notch induces squamous cell differentiation.

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

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

Angiopoietin-like proteins signal through notch via receptor interaction and can regulate Notch cleavage/activation.

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 Notch signaling pathway drives transitions in differentiation capacities during the gradual loss of potency that occurs in the preimplantation mouse embryo before the onset of the first lineage decisions.

Notch signaling alters TLR-induced inflammation by skewing monocyte cell fate toward patrolling monocyte differentiation at the expense of macrophage cell fate.

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.

Mechanical stress plays a cooperative role with Notch in biliary differentiation of liver progenitors, supporting a model of liver development in which biomechanical cues are key inducers of cell fate.

Pairs of spinal cord neurons arising from a shared progenitor get input from and make outputs to mostly different synaptic partners.