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In a mouse model, this study found that LAM/TSC cells invaded the uterus and increased angiogenesis, while anti-EGFR antibody and rapamycin effectively reduced cell presence and blood vessel proliferation.

This study concluded that CNS1-dependent peripheral Tregs do not significantly impact type 1 diabetes in the NOD mouse model, with thymus-derived Tregs being the primary regulators.

This study found that genetic ablation of Tslp in an AEC mutant mouse model reduced skin inflammation and improved survival, suggesting potential therapeutic benefits for AEC syndrome patients.

This study found that the K6/ODC transgenic mouse model is highly sensitive to identifying genotoxic carcinogens, showing 100% concordance with traditional rodent bioassays.

In this study, transgenic mice expressing a truncated form of latent transforming growth factor-β-binding protein exhibited altered hair cycles due to increased active transforming growth factor-β, impacting keratinocyte proliferation and hair cycle phases.

This study found that brindled mottled mice, a model of Kinky hair syndrome, exhibited abnormal development of catecholamine neurons, with increased TH-immunoreactive neurons and altered neurochemical profiles compared to controls.

This study identified the Itpr3 gene as responsible for the tufted hair loss phenotype in the BTBR mouse strain.

This study observed that overexpression of TGF-alpha in transgenic mice led to thicker epidermis and stunted hair growth, particularly in regions with normally thick skin and low hair density.

This study found that human skin grafted onto certain immunodeficient mice resulted in proliferative scars with characteristics similar to human hypertrophic scars, suggesting these models may better represent the condition's natural history.

This study found that introducing the recombinant rat OTC gene into SPF-ASH mice restored normal hair growth and metabolic function, improving symptoms associated with OTC deficiency.

This study observed dynamic behaviors such as cluster formation, migration, and active proliferation of transplanted bone marrow cells in a mouse model, providing insight into cellular-level changes post-transplantation.

This study found that conditional deletion of CD271 in mouse epidermis led to significant disorganization and increased thickness, suggesting CD271's crucial role in regulating skin differentiation and structure.

This study found that over-expression of thymosin beta-4 in transgenic mice accelerated wound healing and hair growth, but did not affect tumor progression despite stimulating tumor metastasis.

In this study, basal cell carcinoma developed in Ptch-deficient mice only after chemical treatment, not skin wounding, suggesting a second unknown event is necessary for tumor formation.

In this study, the researchers observed that inducing and then withdrawing β-catenin expression in a bigenic mouse model caused reversible changes in skin morphology, indicating dependence on β-catenin signaling.

This study demonstrates that mice with ectopic expression of the human GLI-1 gene in their skin developed tumors resembling human basal cell carcinoma, suggesting that GLI-1 is central to tumor development without additional p53 or Ha ras mutations.

Cathepsin L deficiency causes hair and skin issues in mice.

This study developed a testosterone propionate-induced C57BL/6 mouse model of androgenetic alopecia, demonstrating that high-dose, prolonged testosterone administration inhibited hair regrowth and mirrored human AGA pathology, providing a useful platform for studying hair loss mechanisms and testing therapies targeting the Wnt/β-catenin pathway.

This study identified TSC2 as an important regulator of hair follicle morphogenesis and patterning, with Tsc2cKO mice showing altered hair patterns and frequencies compared to controls.

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 found that the retinoid LGD1069 suppressed mammary tumorigenesis in a mouse model without observable toxicity, while TTNPB showed modest effects but was associated with significant toxicity.

This study reports the development of the first rodent model for androgenetic alopecia, demonstrating that overexpression of androgen receptors in mice delays hair regeneration and can be used to test new treatments.

This study found that the development of Merkel cell carcinoma from hair follicles in mice can be driven by in vivo reprogramming with ATOH1 and relies on p53 loss for progression.

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.

In this study, inactivating the TAF4 subunit of transcription factor TFIID in mouse epidermis disrupted gene expression linked to skin and hair function, and increased tumor risk.