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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 found that blocking the hypothalamic-pituitary-gonadal axis in male rats reduced baroreflex dysfunction and inflammation caused by endotoxemia, highlighting potential therapeutic benefits.

This study found that an E-cadherin mutant preserved normal cadherin levels and prevented inflammation and lethality in mouse skin lacking p120, highlighting p120's role in regulating cadherin-mediated cell adhesion and inflammation.

This study reported that deleting the MED1 subunit from the MED complex in keratinocytes resulted in disrupted hair differentiation and cycling, leading to hair loss in mice.

In this study, PKC ε transgenic mice exposed to ultraviolet radiation showed increased hair follicle stem cell frequency and altered gene expression compared to wild-type mice, suggesting a potential role in skin cancer susceptibility.

This study describes various clinical phenotypes associated with FOXN1 mutations, finding that affected individuals may develop different severities of immunodeficiency based on their genetic mutations.

This study used Cisd2 knockout mice models and found that these mice display premature aging characteristics and an increase in dysfunctional neutrophils, suggesting Cisd2's role in calcium homeostasis and neutrophil function via interactions with Calnexin and SERCA.

This study found that ACKR2 plays a crucial role in reducing inflammatory skin fibrosis and promoting inflammation resolution through IFN‐β production, limiting tissue scarring.

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 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.

In this study, the Foxn1(-/-) nude phenotype was associated with an altered regulation of epithelial progeny in skin, offering a valuable model for investigating stem cell niche maintenance and regulation.

This study identified a novel missense MAFB variant in a family with some unaffected members, suggesting incomplete penetrance and the potential influence of modifier genes, epigenetic mechanisms, or environmental factors on MCTO phenotype.

This study reported that knocking out the HR gene in pigs using CRISPR/Cas9 led to hairless eyelids and abnormalities in the thymus and peripheral blood, suggesting pigs as a model for human HR-related hair disorders.

This study found that B6.CD80CD86−/− mice developed autoimmune-like alopecia with nearly 100% incidence by 40 weeks, making them a promising model for studying human alopecia areata.

This study found that Akt2 and SGK3 are crucial for postnatal hair follicle development in mice, as their combined absence led to severe hair growth defects due to disrupted β-catenin-dependent transcriptional processes.

This study reports that the loss of the protein Memo in mice leads to a reduced lifespan and suggests that Memo is a key regulator of FGFR signaling and vitamin D production.

This study found that HtrA2 inactivation in mnd2 mice is associated with delayed hair cycle phases and growth retardation of adipocytes, suggesting HtrA2's role in regulating adipogenesis-related hair growth.

This study established a Krt24-CreERT2 mouse line targeting outer bulge hair follicle stem cells, finding these cells crucial for hair follicle development and repair, particularly following ionizing radiation exposure.

This study reported that the anti-γc antibody hC2 restored hair follicle homeostasis and suppressed hair loss in an AA-like mouse model by inhibiting autoreactive T-cell activity, suggesting that hC2 may offer a safer and more effective treatment for alopecia areata compared to current Jak inhibitors.

In this study, transgenic mice overexpressing the glucocorticoid receptor in certain epithelia showed skin development abnormalities resembling ectodermal dysplasia and exhibited reduced inflammatory responses.

This study reports that the monoclonal antibody BKN-1 specifically stained basal cell epithelioma cells and certain normal skin structures, indicating a similarity in keratin expression between the tumor and follicular epithelium below the isthmus portion.

In this study, blocking the CXCR3 receptor in mice prevented the development of alopecia areata by inhibiting the accumulation of specific T cells in the skin, suggesting a potential therapeutic approach for humans.

This study found that topical treatment with 7DHC and BM15766 reduced hair growth in mice compared to those treated with Ethanol/DMSO, and hair did not recover after treatment ceased, alongside increased apoptotic cells and decreased expression of specific genes.

This study found that the co-ablation of C/EBPalpha and C/EBPbeta in adult mouse skin disrupted sebocyte differentiation and epidermal homeostasis, highlighting their critical roles in these processes.

Mouse Scube3 affects teeth, tongue, vibrissae, and eye development, but not facial structure or limb growth.

This study confirms that zebrafish engineered with Cantú Syndrome mutations in ABCC9 and KCNJ8 genes exhibit gain-of-function characteristics in their cardiovascular KATP channels, similar to mammalian counterparts.

This study demonstrated that elevated glucocorticoid levels in transgenic mice led to pancreatic exocrine cells transforming into hepatocyte-like cells, resulting in pancreatic dysfunction.

In this study using mice with specific gene knockouts, both farnesyltransferase and geranylgeranyltransferase-I were found to be essential for the proliferation and survival of skin keratinocytes.

This study found that FOXN1 haploinsufficiency is a significant genetic factor causing T cell lymphopenia at birth, linked to reduced thymic function in both humans and mice.

This study found that the vitamin D-VDR system is crucial for mineral and bone metabolism post-weaning and identified missense mutations in 1alpha-hydroxylase causing type I rickets.