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In this study, two unique mutations in the RBPJ gene were identified and linked to Adams-Oliver syndrome, confirming impaired DNA binding of mutated RBPJ as a factor in this rare genetic disorder.

In this study, researchers observed that a noncanonical mechanism involving the γ-secretase-dependent, RBPj-independent Notch intracellular domain improves survival in Msx2-Cre mice by delaying hair follicle destruction and reducing disease severity.

This study found that the acceleration of endothelial to mesenchymal transition due to loss of Notch signaling led to delayed wound healing and increased scarring in skin wounds.

This study found that Notch signaling is crucial for maintaining proper melanocyte distribution and preventing premature differentiation in the melanocyte lineage within hair follicles.

In this study, the researchers reported that Notch/CSL signaling is crucial for hair follicle differentiation, with Wnt5a signaling and FoxN1 acting as mediators in mice.