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This research observed that the skeletal abnormalities in Noggin null mice varied based on genetic background, and identified haploinsufficiency leading to joint fusions, similar to human conditions associated with NOGGIN deficiency.

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 suggests that the harlequin ichthyosis mouse model closely resembles human type 2 harlequin ichthyosis, indicating its potential as a useful model for studying the human condition.

This study developed a novel Hairless Rag2/Jak3 KO mouse model, which provides superior optical properties and thinner skin compared to existing models, enhancing its utility for noninvasive tumor monitoring and evaluation of anticancer therapies.

This study suggests that the NCSTN knockout mouse could serve as an HS animal model, with tamoxifen potentially used for gene deletion in mice.

This study found that mice with a homozygous knockout of the Ten1 gene, developed through CRISPR-Cas9-mediated exon 3 deletion, exhibited telomere shortening and symptoms consistent with accelerated aging, such as reduced lifespan, skin changes, aplastic anemia, and cerebellar hypoplasia.

This study presents an improved reference genome for the African spiny mouse, which may aid in understanding its tissue regeneration at the molecular level.

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

In this study, researchers observed that mice with the naked gene showed frequent absence of hair cuticle and cortical cells during follicle growth, with abnormal keratin deposition also noted.

In this study, a transgenic mouse model was used to demonstrate that targeted cell loss in different tissues led to varying degrees of regenerative outcomes, including reversible impaired glucose tolerance, irreversible hair loss, and permanent moderate deafness.

This review details the development and genetic background of senescence-accelerated mouse strains, provides a comprehensive examination of their phenotypes, and highlights their importance for aging research, but reports no new experimental results.

This study established that the Dct::CreERT2 mouse line is effective for targeting and studying adult melanocyte stem cells, contributing to the understanding of melanocyte biology and hair pigmentation.

This study observed that female mice with disrupted 5α-reductase 1 showed increased insulin resistance and hepatic steatosis, suggesting altered glucocorticoid metabolism contributes to metabolic disorders.

This study found that the angora mouse mutation prolongs the anagen phase, resulting in excessively long hair and follicular abnormalities, without involving circulating hair cycle factors.

This article discusses the impact of the tabby mutation on secondary vibrissae and hair follicle patterns in mice and reports no new clinical results.

This study found that bovine slick mutations may enhance heat stress responses in mice but do not lead to the expected hair phenotype changes.

This study identified complex regulatory elements and interactions involving the Hr gene and HR protein that are crucial for hair follicle formation and cycling in mammals.

This review summarizes studies on knockout mouse models revealing abnormalities in skin and hair follicle development but reports no new experimental results; the authors highlight the utility of these models for understanding hereditary skin disorders.

This study identified a new mouse mutation associated with noninflammatory proliferative skin disease and hair abnormalities, drawing parallels to human conditions like Netherton's syndrome and monilethrix.

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.

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 the mutant hairless rhino bald protein in mice interacts with the vitamin D receptor but cannot repress its transactivation and shows abnormal cellular localization.

In this study, transgenic mice overexpressing the SSAT gene were highly sensitive to polyamine analogues, leading to severe liver changes and high mortality rates after treatment.

Mouse embryos can develop in chick embryos, but they grow smaller with some organ issues.

This study found that chronic stress may inhibit hair follicle growth and melanogenesis in mice through modulation of the central HPA axis, with C57BL/6 mice appearing most sensitive to these effects.

This study found that mutations affecting hair keratin expression on Chromosome 15 in mice may cause altered hair and skin features similar to other known mouse mutations.

This study found that MPZL3 plays a crucial role in regulating the hair cycle clock in mice, with its absence leading to accelerated hair follicle cycling and suggesting potential therapeutic pathways for alopecia treatment.

This article describes the "naked" mouse mutation, which results in hair loss and is linked to chromosome 15, noting similarities and differences with human ectodermal dysplasia, but provides no new experimental findings.

This study identifies a new mutation in the Scd1 gene in a strain of Kunming mice, causing skin and hair defects with the mildest impact among similar mutations.

Mutations in the Sgk3 gene cause fuzzy hair in mice.