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.

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

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.

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

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

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.

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

The retromer complex serves as a bomb squad to retrieve and disarm the potentially harmful pool of Notch receptors in a timely manner and thereby safeguards against brain tumor formation.

Antagonistic signaling by the kinases PI3K and Itpkb limits the kinetics and enforces the Notch-dependence of beta-selection – the most important cell-fate determining process in alpha beta T cell development.

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.