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This study reports that transgenic mice carrying Clone B DNA developed spontaneous melanomas likely due to an interruption in genes regulating cell growth in melanin-producing cells, offering a model for melanoma research.

This study found that homozygous mutant mice with a hypomorphic CD18 mutation developed a chronic inflammatory skin disease resembling human psoriasis, potentially implicating additional genetic factors in disease susceptibility.

This study found that deleting transferrin receptor 1 in specific mouse tissues led to varied lethal outcomes, demonstrating its diverse roles beyond iron uptake.

This study in mice suggests that defects in hair follicles with mesenchymal TSC2 disruption may result from an impaired TGFβ1 response, indicating a potential novel treatment approach for tuberous sclerosis complex.

This study found that mice with a disrupted TGFα gene display a curly whisker-coat phenotype, similar to waved-1 mice, suggesting TGFα's crucial role in skin architecture and hair development.

This study presents two new mouse models using the CreER T2-loxP system to target and study melanocytic cells, with implications for melanoma research.

In this study, Sox13 was identified as a novel marker for early hair follicle development and differentiation in mice, though it appears to be dispensable for overall epidermal and adnexal development.

This study found that mimicking the XPD point mutation in mice resulted in trichothiodystrophy-like symptoms, supporting the role of basal transcription and DNA repair defects in the disease.

The Trichodysplasia spinulosa virus protein can cause abnormal hair growth in mice.

In this study, the disruption of Gh/tissue transglutaminase in mice did not affect viability but reduced thymocyte viability and fibroblast adhesion, suggesting its role in cell stabilization and extracellular matrix interactions.

This study successfully established Tsc2-deficient embryonic stem cells from Eker rats and found these cells have distinct gene expression compared to non-mutant cells, which could help identify new therapeutic targets for TSC-related pathogenesis.

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.

This study identified a nonfunctional Itpr3 gene in BTBR mice, attributed to a 12-bp deletion, which likely causes their simultaneous hair loss and taste perception deficits.

Harris et al. describe a new mouse model for vitiligo, where interfollicular melanocytes are retained and melanocyte-targeting immune responses are simulated, aiding the development of immunomodulatory therapies.

In this study, introducing the rat OTC gene into spf-ash mice led to increased OTC activity and normalized hair growth and biochemical markers like urinary orotic acid and serum citrulline, partially correcting the symptoms of OTC deficiency.

This study observed that K5Cre +/+ transgenic mice develop a distinct phenotype characterized by wavy hair, curly whiskers, and an increased rate of papilloma malignant transformation.

This study reports that transgene insertion in homozygous transgenic mice causes irreversible hair loss and impaired immune function, linked to interruption of the hairless locus on Chromosome 14.

In this study, Trf1 genetic deletion in mice, including those with cancer-prone mutations, was shown to not affect overall viability and cause only mild effects, while being necessary for tumor formation, suggesting a potential therapeutic window for Trf1 as an anti-cancer target.

This study observed that NSG-hu-BLT mice developed graft-versus-host disease characterized by CD8+ T lymphocyte-related cell death in the skin and liver, which may affect their utility in other research areas.

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

This study found that introducing rat ornithine transcarbamylase gene into spf-ash mice improved liver and intestinal enzyme activity and normalized some metabolic indicators.

This study found that over- and ectopic-expression of FoxN1 in early life negatively affected the development of thymic epithelial cells, T and B cells, and skin epithelial cells.

This study demonstrated that 5-azacytidine treatment may reduce TSC lesion-related hair follicles in mice, suggesting chromatin remodeling agents could be effective for tuberous sclerosis cutaneous lesions lacking tuberin.

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 successfully created a mouse model with conditional knockout of the p75 neurotrophin receptor gene in epidermis cells, with no significant changes in skin histomorphology observed.

This study developed a foxn1-deficient Xenopus laevis model using CRISPR/Cas9, observing reduced T-cell markers and altered immune responses in tadpoles, providing a nonmammalian model for immunological research.

This study found that conditional expression of TGFβ1 in mice affects epidermal and hair follicle growth, with chronic expression causing severe alopecia and a negative feedback loop involving Smad7.

This study introduced a novel in vitro murine assay using transgenic mice to identify immunomodulatory compounds, which identified 160 potential hits from 4,398 compounds screened.

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 thymus transplantation in athymic mice resulted in T-cell-driven hair follicle depigmentation and loss, without multiorgan autoimmune disease, highlighting mechanisms of tissue-specific tolerance.