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This study observed that some patients with homozygous c.736T>A mutation in LIPH may have mild hypotrichosis with long hairs in adulthood.

A gene mutation in mice causes increased mast cells and disorganized hair follicles in their skin.

This study found that a newly identified mutation in the hairless gene in mice led to decreased Hr mRNA levels and changes in gene expression related to hair follicle development.

This study in mice found that overexpressing Sonic Hedgehog in basal cells caused skin anomalies and a lack of certain hair fibers, underscoring its key role in hair follicle development.

This study found that individuals with heterozygous truncation-type variants in the *DSP* gene exhibit lower skin temperature and higher transepidermal water loss, with specific microscopic skin changes and pseudomonilethrix.

In this study, the misshaped and hairy ear phenotype in mutant mice was linked to mis-expression of certain Hoxc genes due to a chromosomal inversion.

In this study, researchers created a mutant mouse lacking the first cut repeat in the Cux/CDP protein, resulting in curly vibrissae and wavy hair, supporting the role of Cux/CDP's DNA binding domains in gene regulation during development.

This study found that Naked trait mice exhibit a decrease in certain low-molecular-weight proteins in their hair, which contain high levels of glycine and tyrosine, compared to normal mice.

In this study, researchers created a mouse model using CRISPR/Cas9 technology to investigate hypotrichosis simplex and woolly hair, finding that Krt71-knockout mice exhibited curly hair and developed complete hair shedding without immune deficiencies, mimicking conditions seen in humans and potentially aiding future hair disorder research.

In this study, researchers identified a new dominant mutation in Hairless mice, called Pied, resulting from a deletion in the Adam10 gene, which causes freckle-like skin pigmentation by inhibiting melanocyte expansion.

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.

The Thr1022Ala variant in the hairless gene is not a disease-causing mutation.

This study found that maternal hephaestin knockout in mice leads to neonatal hair loss, likely due to low iron levels in the mother's milk.

This study suggested that differences in hair follicle development, indicated by the frequency of underdeveloped hairs, significantly contribute to the variation in hair loss severity among Japanese individuals with the LIPH c.736T>A mutation.

This study identified novel LSS mutations implicated in hypotrichosis simplex with or without neurodevelopmental abnormalities, highlighting the need for careful evaluation of synonymous mutations' potential pathogenic effects.

This study identified two prevalent and one newly proposed founder LIPH mutations in Japanese patients with autosomal recessive woolly hair/hypotrichosis and associated these mutations with different severities of hair loss.

In this study, researchers using a mouse model found that the hairlessness in nude mice is likely due to a shared defect in the thymus and skin, not thymic dysgenesis alone.

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.

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.

This study found that knocking down P-cadherin expression in cultured human hair follicles recreates the hair abnormalities seen in patients with hypotrichosis with juvenile macular dystrophy.

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 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 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.

This study found no qualitative skin differences during development between mutant hairless USP mice and BALB/c mice, except for enlarged cysts in the hairless strain.

This article reviews phenotypic variability linked to WNT10A nonsense mutations and does not present new research findings.

This study identified a missense mutation in the rat Desmoglein 4 gene, causing abnormal hair shaft development in lanceolate hair mutant rats by disrupting a critical calcium binding site.

This study found that hair follicle stem cells in the hairpoor mouse, a model for Marie-Unna hypotrichosis, lose their quiescent state, leading to a disordered hair cycle and contributing to alopecia.

This article reviews the history and characteristics of the rare nude phenotype SCID, primarily distinguished by severe T cell immunodeficiency and notable skin and hair abnormalities, but reports no new clinical findings.

This study found that mutant mice with the we/we wal/wal genotype exhibit significant defects in hair shaft structure and epidermis stratification, correlating with postnatal alopecia symptoms.

Researchers created a new mouse model for studying scleroderma.