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This study found that the AtSfh1 protein in Arabidopsis is essential for phosphatidylinositol-4,5-bisphosphate signaling crucial to polarized root hair growth, utilizing both phosphatidylinositol and phosphatidylcholine-binding activities.

This study identified key regions and transcription factors, including SIX1 and FOXN1 itself, that regulate Foxn1 expression in thymic epithelial cells and hair follicle cells, offering insights into its transcriptional regulation.

This study discovered that calcium dependent protein kinase 1 (CPK1) directly activates cyclic nucleotide-gated channels 5, 6, and 9, promoting root hair growth in Arabidopsis by regulating Ca²⁺ signaling.

In this study on Drosophila embryos, researchers observed that the Slit/Robo signaling pathway is crucial for the collective migration and proper positioning of Posterior Signaling Center cells within the hematopoietic niche, highlighting its role in niche assembly and cellular organization.

This study found that S1PR1 signaling in mouse aortic endothelial cells varied by location and subtype, influencing inflammatory and lymphangiogenic gene expression through distinct molecular pathways.

This study found that targeting S1PR1 signaling in mouse aortic endothelial cells helps suppress inflammation-related gene expression while revealing diverse and spatially distinct endothelial cell subtypes.

This study concluded that terminal Schwann cells are essential for the maintenance and regeneration of mechanosensory lanceolate complexes at hair follicles in adult mice.

This study analyzed skin from 538 knockout mouse mutants and identified 50 with epidermal phenotypes, providing valuable insights into genetic conditions and systemic effects related to skin abnormalities.

This study found that Hoxc13 mutations in mice cause defects in hair, nail, and tongue structures, with the most noticeable issue being brittle hair leading to alopecia.

Hairless mice lack fur due to a genetic mutation affecting skin response, not hormone issues.

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.

This study describes a mouse model for Marie Unna Hereditary Hypotrichosis, identifying mutations in the hairless gene that result in sparse or absent hair and cyst-like hair follicles.

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 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.

This study found that mutations in the hairless gene in mice disrupt hair follicle integrity during catagen, leading to baldness due to disintegrating epithelial structures and loss of normal dermal papilla.

This study reports a case of GGCX syndrome in a 55-year-old Japanese male, characterized by PXE-like symptoms and coagulation deficiency, with an unreported phenotype of possible spinocerebellar degeneration.

This study observed that the hair loss in homozygous rhino mice is associated with widening of the hair canal due to hyperkeratosis, leading to insufficient support for hair anchoring.

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.

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 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.

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 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 identifies iRhom2 as a crucial regulator of hair follicle differentiation, showing that the iRhom2Uncv mutation leads to dysplasia and reduced TACE maturation, resulting in a hairless phenotype in mice.

This study found that expression of certain mutant keratin genes in mice led to severe alopecia, suggesting a similar mechanism could cause hair loss in humans.

This study found that loss-of-function mutations in the HOXC13 gene cause autosomal-recessive pure hair and nail ectodermal dysplasia, emphasizing its role in hair and nail development.

This study identified that in Japanese patients with autosomal recessive woolly hair/hypotrichosis, the c.736T > A LIPH mutation is associated with a mild phenotype, while the c.742C > A mutation may lead to severe baldness.

This study found that a nonsense mutation in the Cst6 gene of mice leads to severe skin and hair abnormalities, suggesting that cystatin M/E is crucial for epidermal function and viability.

This study reported that patients with specific Foxn1 mutations exhibited severe T-cell lymphopenia without the hair and nail abnormalities usually associated with these mutations.

This study identified a homozygous frameshift mutation in the HOXC13 gene associated with pure hair and nail ectodermal dysplasia in a consanguineous Syrian family, suggesting crucial roles for HOXC13 in hair and nail development.

The Dfl mutation in mice causes poor sebaceous gland function and complete hair loss.