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In a keratinocyte-specific knockout mouse model, this study found that deleting GRK2 disrupted hair follicle homeostasis, causing cyst-like structures, abnormal growth patterns, and eventual hair loss, suggesting potential links to immune-mediated alopecias.

This study found that while epidermal PLCγ1 is not necessary for keratinocyte differentiation in interfollicular epidermis, it is crucial for normal hair and sebaceous gland formation in mice.

This study found that the enzyme A20 helps regulate EDAR-induced NF-κB signaling in mice, preventing ectodermal abnormalities like disheveled hair and assuring proper skin and appendage development.

In this study, researchers found that the deletion of Tet2/3 enzymes in mice led to changes in skin development and hair follicle differentiation, ultimately causing hair loss and altered gene expression.

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

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 deleting all three Tet genes in mice led to shorter hair shafts and altered hair types, with associated changes in gene expression and DNA hydroxymethylation.

TRPV1 helps regulate hair growth cycles.

This study found that deleting β-catenin in epidermis-specific VDR knockout mice did not prevent UVB-induced skin tumors, indicating β-catenin does not compensate for VDR's role in tumor suppression.

This study found that the absence of laminin α5 in adult mice's epidermal basement membrane led to keratinocyte hyperproliferation and immune cell changes, affecting hair follicle development through altered growth factor expression.

This study found that COL17 plays a key role in regulating epidermal keratinocyte differentiation and proliferation, influencing the expression of differentiation markers and cellular growth in specific conditions.

This study found that Stat3 removal in keratinocytes of mice impairs healing and disrupts the normal hair cycle, leading to skin ulcers and hair loss as they age.

Deleting Crif1 in mouse skin disrupts skin balance and hair growth.

This study demonstrated that switching aE-catenin to aT-catenin in murine skin substantially rescued hyperproliferative and pre-cancerous conditions, but led to partial baldness, indicating potential functional discrepancies.

This study observed that the loss of H3K9me3, via the ablation of Suv39h1, Suv39h2, and Setdb1 in embryonic mouse epidermis, disrupts skin development processes such as keratinocyte differentiation and hair follicle formation, highlighting H3K9me3's crucial role in epidermal morphogenesis.

This study found that Pannexin 3 plays a crucial role in skin development by regulating the transcription factor Epiprofin, affecting keratinocyte differentiation and hair follicle regeneration in mice.

This study observed that deleting ARNT in keratinocytes of mice reduced zigzag hair production and altered hair follicle differentiation, likely by affecting the expression of specific cyclin-dependent kinase inhibitors.

This review discusses the roles of store-operated Ca 2+ entry proteins in skin cell function and their links to various skin diseases, but it reports no new results.

This review discusses the role of cholesterol homeostasis in hair follicle biology and its potential connections to various hair disorders, but it reports no new findings.

This study found that the distribution of desmogleins is associated with specific types of keratinization and hair anchorage, as well as hypotrichosis.

This study found that MED1 deficiency in keratinocytes accelerates skin wound healing in young mice but delays healing in older mice, suggesting differential roles in epidermal regeneration with age.

This study found that disrupting the inturned gene in developing mouse epidermis halted hair follicle formation due to impaired keratinocyte differentiation, highlighting primary cilia's role in tissue-specific planar cell polarity signaling.

This study explored the molecular biology of skin adaptations in pangolins, revealing that certain genes for lipid synthesis have inactive patterns, while others related to skin function remain intact, suggesting complex evolutionary changes in their skin physiology.

This study investigated pangolin skin genetics, finding that while sweat gland-related genes are not inactivated, several genes related to sebaceous gland function are, which highlights complex evolutionary adaptations in mammalian skin.

This research found that the microtubule catastrophe factor KIF18B plays a crucial role in promoting spindle orientation in keratinocytes, linking this process to cell fate decisions during hair follicle morphogenesis.

This study found that the loss of Smad4 in keratinocytes reduces Dsg4 expression via disrupted BMP signaling, contributing to hair follicle degeneration and alopecia.

This study found that the transcription factor Gata6 plays a crucial role in adult mouse hair follicle regeneration by promoting the renewal and preventing DNA damage of rapidly proliferating progenitor cells.

In this study, researchers found that CD4 is expressed on murine K5⁺ keratinocytes, and its expression is crucial for maintaining epidermal stem cell balance and wound repair capacity, particularly during aging.

This study found that biallelic LSS mutations lead to congenital hypotrichosis and cataracts, with each tissue-specific loss of function observed in mouse models.

This study suggests that the protease HAT-L4 plays a significant role in maintaining epidermal barrier function to prevent body fluid loss, as its absence in mice led to increased fluid loss and higher mortality.