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.

In adult mouse hippocampus, neural stem cell and their progeny communicate via Lunatic Fringe mediated Notch signaling to regulate stem cell quiescence, division, and fate.

T cell receptor and Notch signaling pathways are linked via a novel mechanism involving modulation of the cytoskeleton.

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

DNA binding site architecture promotes Notch transcription complex degradation to sensitize developmental processes requiring long-duration signaling.

Endoplasmic reticulum-associated degradation (ERAD) is a critical protein quality control checkpoint for thymocyte β-slection.

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.

A combination of spatial proteomic and autophagic flux approaches was used to reveal the landscape of turnover of damaged lysosomes, demonstrating a key role for the autophagy receptor TAX1BP1 and its associated kinase TBK1 in both HeLa cells and iNeurons.

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

The cannabinoids cannabidiol, cannabidivarin, and the newly identified 331-18A demonstrate antitumoral effects in Notch1-mutated leukemia, underscoring the potential and complexity of Cannabis as a novel treatment for cancer.