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This study found that conditional knockout of N-WASP in keratinocytes of mice led to skin barrier defects, increased immune cell infiltration, and hyperproliferation of keratinocytes, indicating its crucial role in skin homeostasis.

In this study, Msx-2 knockout mice showed enhanced re-epithelialization and faster wound closure compared to wild-type controls, suggesting Msx-2 may influence skin morphogenesis during wound repair.

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 in mice, knockout of Rac1 and Rac3 in keratinocytes led to reduced white adipose tissue and revealed Rac-dependent paracrine pathways affecting pre-adipocyte differentiation.

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.

This study found that mitochondrial dysfunction due to Crif1 deficiency in hair follicle stem cells significantly slows the hair growth cycle in adult mice but does not impact the maintenance of HFSC populations.

In a conditional knockout mouse model, this study found that loss of the transcription elongation factor SPT6 in basal keratinocytes led to psoriasis-like skin inflammation and delayed wound healing, suggesting SPT6 plays a crucial role in maintaining epidermal immune quiescence by suppressing proinflammatory NF-κB signaling.

This research suggests that the vitamin D receptor may regulate hair follicle cycling and provide genoprotection against skin carcinogenesis through a mechanism independent of 1,25-dihydroxyvitamin D3, based on evidence from mouse models.

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 study found that Plakophilin 1 regulates innate immune responses in keratinocytes by controlling RNA helicase activity, balancing inflammation during epidermal immune challenges.

This study found that mice lacking the type 3 IP(3) receptor in their hair follicles experienced repetitive hair loss and regrowth, indicating disrupted hair-cycle regulation potentially linked to specific signaling pathways.

This study identified a novel recessive mutation in mice causing lethal congenital lamellar ichthyosis, with skin and hair follicle alterations similar to human congenital ichthyoses, linked to a specific genetic defect affecting Fatp4.

This study provides evidence that psychoemotional stress inhibits hair growth in mice by affecting the brain-hair follicle axis, with specific neuropeptides and treatments modulating this effect.

This study reports improved methods for harvesting and processing keratinocytes from plucked human hair, enhancing their utility in generating donor-specific induced pluripotent stem cells more efficiently and reliably.

This study found that RXRα/RARγ heterodimers are necessary for retinoic acid-induced keratinocyte proliferation in the skin, while normal epidermal maintenance does not require RAR-mediated signaling.

This study found that the microRNA miR-22 is a key regulator of the hair cycle, influencing hair loss by promoting the transition from growth to rest phases and repressing keratinocyte differentiation.

This study found that premature hair loss due to stress does not occur in NK-1 receptor knockout or mast cell deficient mice, suggesting a key role for neurokinin substance P and mast cell interaction in stress-related hair follicle changes.

This study found that deleting Ube2n in adult mouse skin leads to inflammation and other skin changes, and identifies IRAK1/4 as potential treatment targets for inflammatory skin disorders.

This review discusses the development and role of corneodesmosin in skin and hair follicle integrity, highlighting findings from mouse models and its connection to genetic diseases, with no new experimental results included.

This study suggests that the down-regulation of 14-3-3 proteins in wild-type keratinocytes, absent in Smad4 mutant keratinocytes, might contribute to the failure of hair follicles to initiate catagen in Smad4 knockout mice.

In this study, Gsdma1/2/3 knockout mice showed reduced epidermal hyperplasia and inflammation when induced by PMA, which was attributed to decreased EGFR-Stat3/Akt signaling due to a decrease in related ligands.

This study provides genetic evidence that desmoglein-1 can compensate for the loss of desmoglein-3 in hair adhesion, supporting the desmoglein compensation hypothesis.

This study found that the orphan protein Plet-1 is expressed in specific keratinocytes of mouse hair follicles and may regulate keratinocyte interactions with inert tissues by affecting migration and adhesion.

This review summarizes studies on knockout mouse models revealing abnormalities in skin and hair follicle development but reports no new experimental results; the authors highlight the utility of these models for understanding hereditary skin disorders.

In this study involving genetically modified rats, researchers observed that specific mutations in the vitamin D receptor affect calcium levels and bone formation, emphasizing the receptor's role in maintaining healthy bone density and its importance in regulating hair cycle and skin health.

This study found that skin microbiota, particularly in wild-type mice, promotes wound-induced hair follicle neogenesis and wound healing, highlighting the potential downsides of routine antibiotic use on skin regeneration.

This study showed that vitamin D receptor gene-deficient rats exhibit hair loss and skin abnormalities due to differences in gene and protein expression patterns, while ligand-independent VDR action is crucial for normal hair cycle maintenance and skin formation.

This review discusses the expanding understanding of TRPV3's role in pain and skin pathology, while highlighting the need for further pharmacological research to fully resolve its functions.

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

In this study, synthetic vitamin D3 analogs stimulated hair growth and formation of normal hair follicles in nude mice, unlike the natural form 1,25 dihydroxyvitamin D3.