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This study reported that UVR induced PKCε phosphorylation of Stat3 in transgenic mice, suggesting a role in enhancing sensitivity to UVR-related skin cancer development.

This review discusses the role of activin signaling in hair follicle formation, hair growth cycling, and skin healing, but presents no new clinical findings.

This study found that MRP3 is induced in wound edge keratinocytes during wound healing and may play a role as a growth or angiogenesis factor in this process and the hair follicle cycle.

In this study, researchers identified two new keratin-associated proteins, hKAP1.6 and hKAP1.7, in human hair follicles, contributing to understanding hair fiber differentiation.

This study suggests that Mrp3 may play a role in both wound healing and the hair follicle cycle as a growth factor and/or angiogenesis factor.

This study found that stable regeneration of pigmented hairs in mice after severe wounding can occur when the wound is made during the anagen stage, influenced by Wnt and Kit signaling pathways.

This study suggests that Merkel cell polyomavirus T antigen-positive cells resembling Merkel cell carcinoma may originate from epithelial cells in human hair follicles, potentially informing future transgenic mouse models for this cancer.

This study examines the interaction between androgen receptor signaling and the β-catenin/Wnt signaling pathway in mouse hair follicles, but reports no clinical results.

This study found that non-cutaneous melanocytes in mice are less sensitive to Kit signaling compared to cutaneous melanocytes, showing dependence on ET3 and HGF signaling.

This study found that CRISPR/Cas9 efficiently edited two cellulose synthase-like genes in spinach, significantly altering root hair growth patterns and suggesting potential for large-scale genome editing in this crop.

In this study, the researchers used a transgenic mouse model to examine how Wnt and Shh signalling impact skin tumour development when BMP is inhibited, finding that inhibiting Wnt and Shh pathways significantly slows tumour formation in these mice.

This study suggests that activating the hexosamine pathway may enhance skin homeostasis, potentially increasing hair follicle stem cells and modifying extracellular matrix components like hyaluronic acid in vitro.

This study found that occlusive dressings on mouse wounds eliminated wound-induced hair neogenesis by upregulating mechanotransduction, which promotes fibrosis, and suppressing Wnt signaling involved in regeneration.

This study developed a transgenic mouse model to explore androgenetic alopecia, finding that inducible COX2 expression led to sebaceous gland changes and hair miniaturization, with reversible effects upon reducing COX2.

Scientists used a special imaging technique to observe that hair follicle regeneration involves cell division and structural changes, mostly in the lower part of the follicle, and that the dermal papilla at the base is crucial for regrowth.

In this study, transgenic mice with Rank expression in hair follicles showed excessive lymph node growth, which could be normalized by neutralizing the overproduced RANKL, underscoring its role in immune system regulation.

In this study, researchers found that depleting mtDNA in mice caused skin wrinkles and hair loss but restoring mitochondrial function reversed these effects, highlighting mtDNA's significant role in skin and hair health.

In this study, transgenic male mice over-expressing the androgen receptor in mesenchymal stem cells showed reduced fat mass and improved glucose clearance, suggesting enhanced androgen sensitivity may alter body composition.

This study reports that versican expression plays a crucial role in maintaining the anagen phase and hair inductive properties, as shown in a transgenic mouse model and hair growth assays.

In their mouse study, Oda et al. found that removing the MED1 gene in the skin led to hair loss and changes in epidermal cell differentiation, indicating MED1's significant role in these processes.

This study found that transgenic mice overexpressing IKZF1 developed lesions similar to alopecia areata, suggesting that Ikaros may play a role in the disease's pathogenesis. Ikaros expression was also higher in human alopecia areata patients compared to controls.

In this study using a transgenic mouse model, Id2 overexpression in hair follicle stem cells prolonged quiescence by affecting gene expression, partly independent from BMP signaling.

In this study, Stat3 activation in transgenic mice led to a decrease in stem cells in the hair follicle bulge, suggesting its crucial role in epidermal growth and stem cell maintenance.

This study found that the effects of the vitamin D receptor on hair follicle cycling in mice are independent of its ability to bind a hormone, with specific domain mutations influencing hair regrowth outcomes.

This study showed that a 2-kilobase upstream region of the mouse keratin 17 gene enables targeted GFP expression in major epithelial appendages of transgenic mice, indicating sonic hedgehog's involvement in its regulation.

This study found that vitamin D receptor presence is vital for normal hair growth in mice, as shown by vitamin D receptor-null mice developing alopecia, while transgenic expression of human vitamin D receptor in these mice restored normal hair growth.

This study found that HPV16 oncogene expression in multipotent epithelial stem cells led to abnormal mobilization, altering their quiescence without affecting other stem cell markers, suggesting a distinct stem cell compartment.

This study found that overexpression of antizyme in MEK-activated transgenic mice reduced skin tumor development and restored normal differentiation of keratinocyte progenitor cells, highlighting the role of polyamines in keratinocyte biology.

This study found that transgenic mice overexpressing human ATF3 showed hyperplastic and dysplastic changes in epithelial tissues, with a high incidence of oral cancer, suggesting potential oncogenic properties of ATF3.

In this study, researchers established that increased expression of the human GLI-1 gene in mouse skin leads to the development of tumors that closely resemble human basal cell carcinomas, without requiring additional mutations in the p53 or Ha ras genes.