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This study found that transgenic expression of COX-2 in mouse basal keratinocytes causes epidermal hyperplasia and certain dysplastic features at specific body sites.

This study found that desmocollin 1 is crucial for strong adhesion and barrier maintenance in the mouse epidermis, with its absence leading to skin and hair issues resembling chronic dermatitis.

This study found that overexpressing Dsg3 in the suprabasal epidermis of transgenic mice resulted in flaking skin and abnormal hair growth, supporting Dsg3's role in regulating epidermal differentiation.

This study found that schizophrenia-derived neurons exhibited impaired differentiation and mitochondrial dysfunction, suggesting a potential link between these factors and neurodevelopmental processes in schizophrenia.

This study found that DHHC13 is crucial for hair anchoring and skin barrier function, with its deficiency in Zdhhc13(skc4) mice leading to cyclic alopecia and skin abnormalities due to cornifelin deficiencies.

Cathepsin L deficiency causes hair and skin issues in mice.

This study identifies KLK14 as a significant factor contributing to hair defects and skin inflammation in a mouse model of Netherton syndrome.

This study describes three adult dogs with sebaceous gland dysplasia, reporting that two showed moderate to marked improvement in symptoms with treatment, though ongoing management is required as the condition cannot be cured.

In this study, transgenic mice expressing Msx-2 developed flaky skin with hyperproliferation and misalignment in epidermal cells, suggesting Msx-2 plays a role in skin and appendage growth control.

This study found that WWOX deficiency in mice leads to impaired skin development, reduced epidermal thickness, and significant hypothermia due to disrupted cell proliferation and homeostasis.

In this study, researchers found that TSPyV T antigens can disrupt normal cell differentiation and proliferation in hair follicles and interfollicular epidermis, possibly contributing to trichodysplasia spinulosa pathology.

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.

In this study, Msx2-deficient mice showed progressive hair loss due to shortened anagen phase and prolonged catagen and telogen phases, resulting in cyclic alopecia with structurally abnormal hair shafts.

This study found that Cutl1 mutant mice experienced retarded lung differentiation and abnormal hair follicle morphogenesis, indicating the vital role of CDP in lung development and hair follicle cell-lineage specification.

This study reports that activating Notch signaling in the hair follicle cortex of transgenic mice caused abnormal differentiation of the medulla and cuticle, highlighting potential cell-cell interactions.

In this study, disrupting the epidermal growth factor receptor in mice led to abnormal hair and skin development, characterized by disorganized hair follicles and systemic disease, providing a model for understanding EGFR's role in skin biology.

This study describes a distinctive form of ichthyosis characterized by abnormal epidermal differentiation mainly within hair follicles in four patients with congenital follicular hyperkeratosis.

This study found that transgenic mice with keratinocyte-specific overexpression of CtBP1 exhibited abnormal hair follicle development, suggesting CtBP1 may play a pathogenic role in hair morphogenesis.

This research found that Dlx3 plays a central role in hair formation and regeneration, with its absence leading to alopecia through disrupted differentiation and signaling pathways.

This study suggests that androgens enhance growth factor production in dermal fibroblasts, which in turn may alter keratinocyte differentiation and contribute to acne lesion formation.

This study found that cathepsin L deficiency in mice led to significant abnormalities in hair follicle development and cycling, including disrupted hair shaft outgrowth and premature hair growth phase entry.

This study found that disrupting Sox21 in developing teeth leads to severe enamel hypoplasia, regional osteoporosis, and abnormal hair formation, with impaired dental epithelial differentiation and regulation of hair follicle cell fate.

This study found that Cathepsin E plays a crucial role in keratinocyte terminal differentiation, affecting epidermis formation and homeostasis in mice.

This review discusses the physiological roles of the epidermal differentiation complex and its potential involvement in psoriasis, but it reports no new experimental findings.

In this study, researchers used single-cell RNA sequencing to define and locate three distinct cell states of melanocytes in mouse skin development, potentially aiding the understanding of abnormal melanocyte differentiation.

This study developed a mouse model to mimic PHGDH gene copy number gain, finding that increased PHGDH expression leads to abnormal melanin production, which may offer insights into its role in melanoma.

In this study, the authors concluded that the TS-associated polyomavirus may disrupt Wnt/β-catenin signaling, likely contributing to abnormal hair follicle formation in trichodysplasia spinulosa.

This study found that overexpression of Claudin 6 in mice led to incomplete epidermal formation and hair abnormalities, suggesting its crucial role in skin differentiation and hair follicle development.

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

In this study, loss of epidermal Par3 in mice disrupted the skin barrier and affected cell differentiation and stem cell maintenance, highlighting its role in epidermal homeostasis.