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This study found that transgenic mice expressing a mutant CYLD protein lacking deubiquitinase function showed signs of premature aging and spontaneous tumor development, likely due to over-activation of specific molecular pathways and chronic inflammation.

This study reported that transgenic mice with targeted TNF alpha expression in keratinocytes showed impaired weight gain, retarded hair growth, and skin changes, leading to cachexia and necrosis.

In this study, nestin-expressing cells in the hair follicle bulge, marked by GFP in transgenic mice, were identified as progenitors of the hair follicle outer-root sheath.

This study found that transgenic mice expressing IGF-1 in their skin showed significant skin changes, early hair follicle generation, and a higher propensity to develop tumors after chemical promotion, suggesting IGF-1's role in skin carcinogenesis.

This study reports that overexpression of activin in transgenic mice enhances granulation tissue formation during wound healing, highlighting a novel role for activin in cutaneous repair processes.

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 suggests that β-catenin plays an important role in wool follicle development in transgenic sheep by enhancing the expression of keratin protein genes.

This study suggests that nestin-expressing hair follicle stem cells, when transplanted into transgenic mice with sciatic nerve injury, can differentiate into motor neurons and reduce muscle atrophy.

This study found that profilin1 protein significantly accelerated wound healing in transgenic mice by reducing wound size and enhancing vascularization and cell migration compared to nontransgenic and 88R/L mice.

In this study, transgenic mice with a truncated latent transforming growth factor-beta-binding protein showed reduced keratinocyte proliferation and alterations in the hair cycle due to mis-localization of transforming growth factor-beta.

In this study, the presence of the HPV11-E2 protein in transgenic mice was found to increase and vary the expression of a reporter gene in hair follicle bulge regions.

This study suggests that the COX-2 enzyme plays a role in hair follicle biology, as transgenic overexpression in mice induced hair follicle cycling disturbances and alopecia, which was mitigated by COX-2 inhibition.

In this study, researchers found that tubular VCAM1 expression in transgenic mice and human kidney transplant biopsies precedes nephron loss and fibrosis, indicating its potential as an early biomarker for tubular fate and adverse kidney outcomes.

This study found that transgenic mice overexpressing the BMP antagonist noggin showed increased hair follicle size and altered hair type, linked to changes in cell proliferation and gene expression.

In this study, hair follicle stem cells from ND-GFP transgenic mice were observed to be pluripotent, effectively repairing peripheral nerve and spinal cord injuries in mouse models.

This study found that controlling transferrin receptor expression effectively regulates iron content in the epidermis and hair of transgenic mice.

This study found that induced COX-2 expression in adult transgenic mice led to hair follicle miniaturization and enlargement of sebaceous glands, and suggests that targeting the PGD2 pathway might reverse these effects.

This study found that an inter-hair-follicle blood vessel network, originating from ND-GFP-expressing stem cells, contributes to angiogenesis in skin transplants and wound healing in ND-GFP transgenic mice.

This study in a transgenic mouse model found that repressing overexpression of ornithine decarboxylase reduced papilloma development, indicating its role in tumor promotion sensitivity.

This study found that high levels of human cytokeratin 16 expression in transgenic mice lead to skin lesions and altered keratinocyte structure, suggesting potential implications for human skin disorders and wound healing.

This study found that transplanting adipose tissue into the rat dorsum supported long-term skin expansion by enhancing thickness, vascularization, and cell proliferation, with adipose-derived cells actively contributing to skin regeneration and growth factor expression.

This study found that a truncated region of the K5 promoter directs expression in stratified epithelia, particularly in epidermis, hair follicles, and tongue, potentially involving specific keratinocyte nuclear proteins in regulation.

This study found that as few as 90 base pairs of the K5 promoter directed keratinocyte-preferred expression in stratified epithelia, especially in epidermis, hair follicles, and tongue, showing cell type specificity.

In this study, researchers discovered that HEY2+ dermal papilla cells exhibit stemness and contribute to dermal regeneration during wound healing, as shown by the expression of a reporter gene in regenerated dermal cells of tamoxifen-induced transgenic mice.

In this study, K19-lacZ transgenic mice exhibited epithelial-specific reporter gene expression in tissues such as the pancreas and stomach, suggesting the K19 promoter is a valuable tool for studying epithelial cell biology.

This study used transgenic mice to show that disrupting TGF-β signaling in K14+ progenitor cells led to increased stem cell proliferation in the tongue.

This study suggests that Foxn1 expression in keratinocytes influences pigmentation in mice, highlighting differences in the molecular mechanisms between mouse and human pigmentation processes.

This study suggests that over-expression of Sp2 may limit stem cell differentiation and contribute to tumorigenic cell growth in mice.

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.

In this study, transgenic mice expressing a mutant K6 gene developed progressive scarring alopecia and keratosis, suggesting they may model a new keratin disorder.