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This study found that follistatin and activin interactions are important for hair follicle development and cycling in mice, suggesting that they may regulate processes involving BMP-2 and its antagonist.

This study showed that knocking out the Ppp2ca gene in the epidermis of mice led to significant hair loss and disrupted hair follicle morphogenesis and regeneration.

This study revealed that frizzled 3 can fully rescue polarity defects in frizzled 6-null mice, while frizzled 6 can partially rescue defects in frizzled 3-null mice, highlighting conserved signaling roles in these proteins.

This study found that in mice, the epidermal microenvironment reverses the oncogenic effects of GNAQQ209L in melanocytes, inhibiting their survival and proliferation through paracrine signals.

This study identified histologic lesions and a defect in adhesion molecules causing hair loss in mice with the bal mutation, linked to a mutation in the desmoglein 3 gene.

This study found that GNAQQ209L expression in mouse melanocytes led to reduced survival in the interfollicular epidermis due to paracrine signaling, while GNAQQ209L boosted survival in a different microenvironment.

This study found that the Gsdma3 gene is necessary for normal hair follicle differentiation in mice, with its mutation leading to progressive hair loss and defects in hair structure.

This study established a Krt24-CreERT2 mouse line targeting outer bulge hair follicle stem cells, finding these cells crucial for hair follicle development and repair, particularly following ionizing radiation exposure.

This study observed that knocking out the 1α-hydroxylase gene in mice resulted in rickets and growth retardation, demonstrating the enzyme's crucial role in vitamin D function in animals.

This study reports a case of GGCX syndrome in a 55-year-old Japanese male, characterized by PXE-like symptoms and coagulation deficiency, with an unreported phenotype of possible spinocerebellar degeneration.

This study identified a novel recessive mutation in mice causing lethal congenital lamellar ichthyosis, with skin and hair follicle alterations similar to human congenital ichthyoses, linked to a specific genetic defect affecting Fatp4.

This study found that fibroblast growth factor 9, initially secreted by γδ T cells, plays a key role in modulating hair follicle regeneration in mice after skin wounds.

This study found that Fos protein expression is closely linked to epithelial cell differentiation, particularly during cornification and cell death, with overexpression observed in keratinization-blocked mutant epidermis.

In this study, researchers observed distinct morphological differences in hair follicles of mutant mouse genotypes, influenced by the expression levels of keratin2-6g, which is essential for proper hair follicle development.

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.

In this study, researchers observed that spontaneously mutated mice with a hair loss phenotype exhibited significant differential expression of genes related to keratinization and hair follicle formation, suggesting these mice could model human alopecia for future research and treatment development.

In this study, researchers identified two distinct homozygous mutations in the KRT85 gene among consanguineous Pakistani families with pure hair and nail ectodermal dysplasia, highlighting variations in severity and potential impacts on the K85 protein function.

This study found that overexpression and knockdown of DKK4 influence genes involved in hair follicle growth and development in Angora rabbits and identified specific SNPs in DKK4 associated with wool quality, notably showing that the TT/GG haplotype combination relates to higher fibre diameters.

This study found that transgenic mice expressing cgVEGF164 had increased hair follicle diameter and density, potentially linked to higher phosphorylation levels of ERK1/2, AKT1, and LEF1 proteins.

This article discusses a novel mutation in the FERMT1 gene identified in a Spanish family with Kindler’s syndrome but reports no new clinical results.

This study suggests that mutation-targeted siRNA therapy could potentially treat keratitis-ichthyosis-deafness syndrome by selectively reducing harmful GJB2 mutant gene expression in patient-derived keratinocytes.

This study found that a newly identified gene, mK17n, may explain the lack of nail issues in mK17 null mice by compensating for mK17's function in the nail bed.

This study identified a mutation hotspot in the caracul (Ca) locus of mice, implicating the mK6irs1/Krt2-6g gene in hair formation and potentially human hair and skin diseases.

This source provides procedural details without reporting new experimental findings or conclusions.

In this study, researchers found that punch grafting was more effective than follicular hair transplantation for treating stable vitiligo; however, follicular hair transplantation was found to be cosmetically preferable for exposed areas like the face due to fewer side effects.

This study found that mutations in the Foxn1 gene in nude mice affect not only hair but also nail structure and differentiation, offering insights into nail hypergranulosis pathogenesis relevant to human nail diseases.

This study found that in mice lacking EGFR, elevated Wnt signaling disrupts hair follicle development by affecting cell proliferation and differentiation, revealing a critical role for EGFR in regulating these processes.

This study suggests that FGF-9 treatment may improve cardiac function by reducing vascular apoptosis and enhancing angiogenesis in infarcted hearts of both nondiabetic and diabetic mice.

This review discusses five genetic fate mapping methods used to study cell behaviors during development and regeneration, detailing the necessary tools and considerations without reporting new experimental results.

This study identifies KLK14 as a significant factor contributing to hair defects and skin inflammation in a mouse model of Netherton syndrome.