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Delta1 is crucial for controlling skin cell growth and preventing tumors in mice.

This study found that Notch-related genes, including Notch1 and Notch2, and their ligands and regulators, have distinct patterns of expression during mouse hair vibrissa follicle development and the adult hair cycle.

This study suggests that cutaneous lymphadenoma is a distinct benign lymphoepithelial tumor characterized by androgen receptor expression, hair follicle stem cell markers, and common EGFR gene mutations.

In this study, loss of the Notch ligand Jag2 in mouse epidermal cells disrupted early differentiation and affected the structure and behavior of adjacent melanocytes, highlighting Jag2's role in epidermal differentiation and tissue homeostasis.

This study suggests that Notch1 acts as a key signal in skin epithelium, promoting immune cell recruitment and aiding in normal skin repair after damage.

This study found that the Notch signaling pathway is suppressed in basal cell carcinomas and highly expressed in hair follicles, suggesting it might be a target for treatment strategies.

In this study, researchers investigating the Drosophila testis niche system reported that Notch signaling is crucial for niche cell specification, with early gonadogenesis showing signals coming from outside the gonad to direct cell fate.

This study reports that in mice, retinoic acid mediates communication between hair follicle and melanocyte stem cells by influencing differentiation in their shared niche during hair regeneration.

In this research, authors found that skin-resident ILCs regulate sebaceous gland function and microbial balance, emphasizing an immune-epithelia system that supports host-microbe symbiosis.

This study found that loss of integrin-β4 or its ligand, laminin-α3β3ɣ2, in keratinocytes increases differentiation via delamination, and demonstrated a role for hemidesmosomes in epidermal differentiation through both mitotic and non-mitotic mechanisms, influenced by Notch signaling.

This study found that Notch signalling promotes differentiation of epidermal cells and acts as a tumour suppressor in the skin by interacting with various pathways and mechanisms.

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 suppressing Jagged1 in epidermal stem cells disrupted Notch signaling and resulted in poor-quality wound healing, suggesting a potential therapeutic target for improving wound repair.

This review explores the role of JAG1 in disease treatment, highlighting the need for effective methods to deliver JAG1 in its bound form to activate NOTCH signaling for therapeutic applications in craniofacial bone loss and myocardial infarction.

This study found that activation or inhibition of Wnt/β-catenin and Notch signaling pathways in rats can alter wound healing, possibly by affecting epidermal stem cell activity and keratinocyte behavior.

This study found that combining platelet-rich plasma with adipose-derived mesenchymal stem cells significantly improved diabetic wound healing in rats by enhancing angiogenesis and modulating the Notch signaling pathway.

In this study, epidermal Notch activation increased jagged 1 expression, leading to skin changes like thickening and blistering, with these effects inhibited when jagged 1 was absent.

In this study, the activation of Notch1 signaling in keratinocytes was found to play a key role in recruiting immune cells and facilitating skin repair after injury.

This study found that the JMJD3/NF-κB-Notch1 pathway plays a crucial role in regulating keratinocyte migration and skin wound healing, with Notch1 affecting key genes involved in cell migration.

This study found that the transcription factors Msx2 and Foxn1 are crucial for maintaining Notch1 expression in the hair follicle matrix, which is necessary for proper hair differentiation.

This study reports that Lef1 plays a crucial role in promoting bulge stem cell differentiation towards hair fate by activating β-catenin and downstream signaling pathways during hair follicle development.

This study found that disrupting Adam10 in the epidermis led to severe skin and multi-organ abnormalities, implicating Adam10 as crucial for proper Notch signaling and skin maintenance.

In this study, pantothenic acid at 20 μg/ml was observed to promote dermal papilla cell proliferation and migration, likely through up-regulation of ID3 and inhibition of Notch signaling.

Hair follicle samples effectively show how well the drug MK-0752 targets and engages with the Notch pathway.

In this study, researchers overexpressed Lrig3 in mouse skin and observed hair loss linked to changes in skin protein profiles and signaling pathways, suggesting a potential role for Lrig3 in maintaining skin homeostasis.

This study found that two microRNAs, oar-miR-23b and oar-miR-133, inhibit the development of hair follicles in superfine wool sheep by targeting genes involved in key signaling pathways, suggesting their potential use as molecular markers for breeding fine wool sheep.

This study observed that the NOTCH signaling pathway may contribute to the development of fibrosis in systemic sclerosis by affecting epithelial cell changes, and inhibiting this pathway could prevent fibrosis in experimental models.

In this study, researchers found that Notch signaling is crucial for late-stage epidermal differentiation and postnatal hair cycle homeostasis by regulating hair follicle stem cell proliferation and differentiation.

This study demonstrated that in mice, the absence of Jagged-1 expression in skin-resident regulatory T cells significantly delays wound healing by reducing the accumulation of neutrophils, highlighting the role of Jagged-1 in coordinating immune cell recruitment during injury.

This review discusses the role of Notch signaling in skin diseases such as Hidradenitis Suppurativa and Psoriasis, but reports no new clinical results.