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

Live-imaging of Notch-dependent transcription in vivo reveals that cell movements during gastrulation influence transcription levels, and do so downstream of Notch cleavage, illustrating the importance of crosstalk between mechanics and transcription in the context of embryonic development.

Foxj1a makes cilia ultrastructurally motile, while Notch signalling stops cilia movement in Kupffer's vesicle.

The conserved mechanism of Notch down-regulation by endo-lysosomal trafficking plays important roles in the proliferation and differentiation of stem and progenitor cells during embryogenesis or organogenesis in vertebrates.

Cell-cycle-dependent Notch signaling cooperates with temporal transcription factors to promote the progression of the temporal transcription factor cascade in Drosophila medulla neuroblasts.

Elucidation of GLI1-Notch1 axis as key determinant of racial disparity in TNBC growth in African American and White American women.

Inhibition of Notch signaling through the Jag2 ligand, blocks homeostatic sebocyte differentiation, and pushes the cells to a progenitor fate, in a reversible manner.

Activation of NOTCH signalling in different cell lineages of the embryonic murine pituitary uncovers an unexpected differential sensitivity, and this consequently reveals new aspects of endocrine lineages development and plasticity.

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

The melanoma cell interaction with lymphatic endothelial cells promotes melanoma metastasis by inducing a reversible switch to invasively sprouting melanoma cells.