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In this study, a mouse model with a PIK3CA gain-of-function mutation in Schwann cells revealed unique communication with neighboring cells and a glycolytic shift in peripheral nerves, and early alpelisib treatment significantly improved symptoms, though efficacy declined with delayed administration due to limited drug penetration.

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

This study observed that Cyp27b1−/− mice exhibited growth and skeletal abnormalities similar to those of Vdr−/− mice, despite differences like the development of alopecia in Vdr−/− mice, suggesting that 1α,25D3 may directly influence chondrocyte proliferation and differentiation.

This study observed that while betaine supplementation decreases total homocysteine and increases methionine levels in a mouse model of CBS deficiency, it is not as effective as methionine restriction in reversing associated phenotypes.

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 high doses of TCB caused severe toxicity in cotton top marmoset monkeys, with clinical and histological changes similar to those in humans and other primates exposed to PCBs.

This study found that inhibiting PKC-β activity with bisindolylmaleimide reduces pigmentation in the skin and hair of guinea pigs and mice by preventing tyrosinase activation.

This study found that deleting Ube2n in adult mouse skin leads to inflammation and other skin changes, and identifies IRAK1/4 as potential treatment targets for inflammatory skin disorders.

This study found that platelet-secreted chemokines like CXCL7 are crucial for early neutrophil recruitment and efficient muscle regeneration in injured mice.

In this study, circ-Smad5 was found to inhibit the proliferation and cell cycle progression of JB6 cells by suppressing Wnt/β-catenin/Lef 1 signaling activation, marking the first report of its function.

This study found that Dab2 conditional knockout mice experienced delayed hair follicle cycles and reduced hair follicle stem cell activity, suggesting Dab2's crucial role in regulating stem cell activation and anti-aging process in hair follicles.

This study in hairless rats suggests that the deletion of specific hair keratin genes contributes to hypotrichosis and highlights the strain's potential as a model for hair follicle research.

This study found that the hair interior defect in AKR/J mice is linked to a mutation in the Soat1 gene, which disrupts SOAT1 protein expression and affects lipid metabolism critical for normal hair formation.

This study found that Prdm1 is crucial for whisker development in mice, affecting multiple signaling pathways and possibly playing a role in primates' evolutionary loss of vibrissae.

This study found that the protein CCN2 in dermal papilla cells is a physiologically relevant suppressor of hair follicle formation by destabilizing β-catenin, which may help maintain stem cell quiescence.

In this study, knockout of B-raf and C-raf genes in mice showed they are not needed for early melanocyte development, but are crucial for maintaining melanocyte stem cells, as evidenced by hair graying due to stem cell depletion.

This article reviews the genetic basis, diagnostic approaches, and treatment options for nude severe combined immunodeficiency, but does not present any new research findings.

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 CTCF is crucial for proper skin and hair follicle development in mice, affecting keratinocyte differentiation and gene expression in keratin loci.

Removing GRK2 in skin cells causes hair loss similar to immune-related alopecia.

This study found that the wavy coat trait in Nakano cataract mice is polygenic, involving major and minor genes, and resembles human curly scalp hair associated with the PRSS53 gene alteration.

This study found that epidermal-specific deletion of aPKCλ in mice disrupted hair follicle stem cell quiescence and regeneration, leading to abnormal hair cycling and skin changes.

This study found that mitochondrial dysfunction due to Crif1 deficiency in hair follicle stem cells significantly slows the hair growth cycle in adult mice but does not impact the maintenance of HFSC populations.

Martin-Perez et al. show that rapamycin's beneficial effects in a mouse model of Leigh syndrome are linked to the downregulation of protein kinase C.

This study found that overexpression of the mineralocorticoid receptor in a mouse model led to premature epidermal barrier development, keratinocyte apoptosis, and postnatal alopecia, indicating new roles for MR signaling in skin physiology.

This study found that the hairless mutant gene in C 57BL/6 mice affects the hair follicle cycle and leads to early thymus degeneration and distinct skin changes.

This study reported the creation of isogenic immortalized COL7A1-deficient keratinocyte lines, providing a model for researching Recessive Dystrophic Epidermolysis Bullosa biology and potential therapies.

This study reports that the nuclear receptor co-repressor 1 (NCoR1) inhibits cardiac hypertrophy by stabilizing the MEF2 and class II HDACs complex, potentially offering a target for new therapies.

This study found that combined loss of Atr and p53 in adult mice led to severe tissue degeneration and delayed regeneration due to the accumulation of highly damaged cells.