Notch signaling controls the collective migration of parapineal cells through its capacity to restrict FGF pathway activation to a few leading cells.

Activation of Notch receptors by ligands in the same cell (cis-activation) is a prevalent and functional mode of signaling in the Notch pathway, and co-exists with trans-activation and cis-inhibition.

The Notch signaling pathway can use its various ligands, receptors, and Fringe proteins to generate diverse intra- and intercellular signaling behaviors.

Tgfb3 inhibits Muller glial cell reprogramming and drives Muller cell quiescence in the injured zebrafish retina, thereby inhibiting retina regeneration.

Hairless emerged as an evolutionarily novel regulatory protein that replaced an ancestral paradigm of direct co-repressor recruitment by Suppressor of Hairless, its partner transcription factor in the Notch signaling pathway.

Notch ligands expressed in the same cell as the Notch receptor are crucial to prevent accidental, ligand-independent Notch activity.

Fringe proteins modulate cis inhibitory, same-cell interactions between the Notch receptor and its ligands to control whether, and in which direction, cells can signal to one another.

The Notch signaling pathway has a central role in the formation of the circuit that controls egg-laying in the nematode worm C. elegans.

C. elegans germline stem cells become quiescent under starved conditions, and this quiescence maintains the stem cell state even in the absence of GLP-1/Notch signaling, which is otherwise essential for stem cell maintenance.

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