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This study created transgenic mouse models with the LMNA gene mutation common in Hutchinson-Gilford progeria syndrome, revealing skin and teeth abnormalities related to transgene expression levels.

This study identified that a deficiency in the palmitoyl transferase enzyme, due to a mutation in the Zdhhc13 gene, led to severe physiological abnormalities in mice, including skin, bone, and systemic amyloid issues.

This paper discusses two preclinical models for studying alopecia areata and finds that testing new therapeutic agents should involve both the C3H/HeJ mouse model and the humanized mouse model for comprehensive insights.

This study found that a mutation causing Stormorken syndrome in mice led to skeletal abnormalities and unusual hair growth, showcasing the STIM1 R304W protein’s role in bone development and cell fate.

This study found that supplementing pregnant and lactating mice with high dietary copper improved survival and physical traits in mice carrying the crinkled mutation, suggesting copper's role in modulating gene expression.

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 found that defective cross-linking in hair cuticles is observable in a minority of mouse hair mutants, suggesting different proteins are involved in cross-linking across cell types.

In this study, researchers identified a mutation in mice that causes hair loss and immune system issues, located on chromosome 18.

This study found that mutant cells in hair follicles can be tolerated or eliminated by surrounding normal tissue, suggesting the potential for wild-type cells to counteract oncogenic mutations.

This study found that the hairless gene in mice has a more extensive role in development than previously thought, as indicated by its expression in various tissues and associated abnormalities in hr/hr mutants.

Krt6a-Cre transgenic mice help study gene effects on hair follicle development and tumor suppression.

This study identified that patients with compound heterozygous mutations in FOXN1 exhibited severe T-cell lymphopenia but retained normal hair and nail development, indicating a distinct clinical phenotype from classic FOXN1 cases.

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 study observed that hairless mice of different strains initially grow hair but soon develop alopecia and other skin and pigmentation changes with age.

This study found that transgenic mice overexpressing human H-ferritin showed mild growth retardation and a temporary hairless phenotype, highlighting H-ferritin's physiological roles.

This review discusses genetically-engineered mouse models for studying melanocytes and reports no new experimental findings; it emphasizes their potential to address unanswered questions in melanoma biology.

This study created a humanized mouse model of hereditary vitamin D-resistant rickets that lacks alopecia, indicating the mutant receptor's potential to explore the syndrome's characteristics beyond vitamin D binding.

In this study, researchers developed a new photoactivatable Cre recombinase mouse model, DiLiCre, which allows precise light-induced genetic modifications and cell tracing, demonstrating its effectiveness for advancing biological and biomedical research.

This study observed that PCR-based genotyping for cre-loxP mice can lead to errors due to cre-mediated recombination in non-target tissues like tails, affecting the detection of lox alleles.

In this transgenic mouse study, preliminary findings suggest that overt melanocyte hyperplasia may require prior keratinocyte hyperplasia, indicating a potential role for keratinocyte mutation in early melanoma development.

This study suggests that biallelic loss of the Hedgehog signaling repressor Patched alone in Keratin 5+ epidermal cells is insufficient to drive basal cell carcinoma development unless exogenous stimuli trigger accumulation of BCC precursor cells.

This study found that benign tumors with a high risk of malignant progression primarily arise from hair follicle cells when a mutant ras gene is expressed in a specific population of epidermal cells in mice.

This study found that mutations in type I IRS keratin genes disrupt keratin protein complexes in mice, suggesting crucial roles for these genes in proper hair coat formation.

This study found that Hoxc13-/- rabbits exhibit complete hair loss on the head and dorsum, providing a potential model for understanding human ECTD-9 and related dermatological conditions.

In this study, a missense mutation in the MAP2 gene was found to be associated with reduced hair follicle density, leading to the hairless phenotype in pigs.

This study developed the mTurquoise2-Col4a1 mouse model and used fluorescent tagging of collagen IV to offer new insights into basement membrane dynamics during hair follicle budding, revealing that basement membranes are flexible and stable structures in developing skin tissue.

This study found that mice genetically modified to overexpress the serine protease inhibitor hurpin showed reduced UV-induced apoptosis but increased susceptibility to skin cancer after chemical carcinogenesis.