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This study found that conditional deletion of CD271 in mouse epidermis led to significant disorganization and increased thickness, suggesting CD271's crucial role in regulating skin differentiation and structure.

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.

This study found that mice with a specific loss of DNA methyltransferase 1 showed uneven epidermal thickness, reduced hair regeneration, and progressive alopecia, emphasizing DNA methylation's role in stem cell homeostasis.

This study demonstrates that Rac1 activity is essential for normal hair follicle formation but influences hair structure and pigmentation, in terminal differentiation, through alterations in hair shaft, cuticle, and pigmentation organization.

In this study, researchers observed that a noncanonical mechanism involving the γ-secretase-dependent, RBPj-independent Notch intracellular domain improves survival in Msx2-Cre mice by delaying hair follicle destruction and reducing disease severity.

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

In this study, Lrig1-positive stem cells in mouse hair follicles were found to be essential for sebaceous gland formation and maintenance, with their depletion causing a temporary loss of these glands and changes in cellular differentiation.

This study found that miRNA biogenesis, facilitated by Dicer and Drosha, is crucial for adult hair follicles' growth and regeneration, highlighting their multiple roles during the hair follicle growth cycle.

TEDAR is crucial for skin cell differentiation and barrier formation.

This study found that the deletion of Med1 in dental epithelia causes a shift from dental to hair tissue development, suggesting the importance of Med1 in maintaining tissue-specific lineage.

This study found that deleting the vitamin D receptor from specific stem cells in mouse hair follicles disrupts their ability to regenerate the epidermis after injury, suggesting an essential interaction with the transcription factor p63.

This study found that LSD1 is crucial for embryonic skin barrier formation in mice, revealing its significant role in epidermal development and suggesting its potential as a target in skin diseases with barrier defects.

This study found that epidermal-specific deletion of aPKCλ in mice disrupted hair follicle stem cell quiescence and regeneration, leading to abnormal hair cycling and skin changes.

In this study, targeted deletion of the stearoyl-CoA desaturase 1 gene in mice disrupted the epidermal lipid barrier, leading to increased water loss, impaired thermoregulation, and metabolic issues.

This study found that MED1 plays a role in maintaining keratinocyte quiescence and hair follicle stem cell populations, as its absence in mice led to increased keratinocyte proliferation and reduced stem cell numbers.

The researchers reported that disrupting ATRA signaling by deleting RDHE genes in the hair follicle led to altered hair follicle cycles, composition, and gene expression, indicating RDHEs' role in hair follicle signaling coordination.

This study introduced Scd3-Cre mice, which enabled sebocyte-specific manipulation, revealing that sebaceous lipid depletion impaired water repulsion, thermoregulation, and the ocular surface, resembling Meibomian gland dysfunction.

This study reported that in mouse models, deletion of EGFR resulted in stem cell hyper-proliferation followed by apoptosis, leading to scarring alopecia, and implicated EGFR's role in maintaining hair follicle quiescence and immune privilege during inflammation.

This study observed that epidermal-specific deletion of aPKCλ in mice disrupts hair follicle stem cell quiescence, leading to altered hair follicle cycling and skin anomalies.

This study found that epidermal-specific deletion of integrin α3β1 significantly reduces papilloma formation in a skin carcinogenesis model by modulating HB stem cell behavior and CCN2 expression.

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.

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

In this study, the researchers found that deleting ceramide synthase 4 in the skin's epidermis alters stem cell differentiation, disrupting hair follicle structure and barrier function, potentially leading to immune responses similar to atopic dermatitis.

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 Rac1 is crucial for maintaining the integrity of hair follicle structure but is not needed for skin epidermis maintenance in mice.

This research observed that EGFR activity appears to maintain hair follicle quiescence and immune privilege, and its inhibition may lead to stem cell apoptosis and scarring alopecia during inflammation.

This study found that the HoxC gene cluster plays a critical role in the development of ectodermal organs, including hair and nails, with mammalian-specific enhancers increasing transcription levels during development.

This study found that loss of integrin-β4 or its ligand, laminin-α3β3ɣ2, in keratinocytes increases differentiation via delamination, and demonstrated a role for hemidesmosomes in epidermal differentiation through both mitotic and non-mitotic mechanisms, influenced by Notch signaling.

This study found that loss of epidermal PPARγ in mice altered the expression of many genes related to skin inflammation, keratinization, and sebaceous gland function, indicating its key role in maintaining skin homeostasis.

In this study, researchers found that coordinated intercellular Ca2+ signaling among basal stem cells in mice is crucial for cell cycle progression and tissue-wide communication during epidermal regeneration.