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This study showed that knocking out the Ppp2ca gene in the epidermis of mice led to significant hair loss and disrupted hair follicle morphogenesis and regeneration.

This study found that Acvr1b signaling is crucial for both hair follicle development and cycling in mice, with the genetic disruption leading to hair loss and a thickened epidermis.

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 this study, Mpzl3-/- mice developed severe seborrhea-like dermatitis with skin inflammation, indicating MPZL3's role in the skin condition's development, independent of adaptive immunity.

This study found that human skin grafted onto certain immunodeficient mice resulted in proliferative scars with characteristics similar to human hypertrophic scars, suggesting these models may better represent the condition's natural history.

EBF1 controls hair type and length.

This research investigated the role of EphA1 in embryonic and adult tissues, generating mouse models suggesting potential links to skin and colon cancer, sepsis, and post-traumatic injury.

This research found that Foxc1 transcription factor and COL17A1 are critical in regulating quiescence and hair thinning in hair follicle stem cells, with aging-related DNA damage leading to hair loss.

This study found that many effects previously thought to be caused by circadian rhythm disruption in Bmal1 knockout mice are actually due to BMAL1's properties unrelated to its clock function.

This study found that activation of cannabinoid 1 receptors in human scalp hair follicles may limit excessive mast cell activation and maturation, suggesting a potential therapeutic strategy for managing MC-dependent skin diseases.

This study successfully created a mouse model with conditional knockout of the p75 neurotrophin receptor gene in epidermis cells, with no significant changes in skin histomorphology observed.

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.

This study suggests that impaired VDR signaling in mice leads to dysregulated Ddit4 expression, impacting hair cycle progression and wound healing.

The study found that in mice, conditional knockout of p53 in epidermal keratinocytes reduced food intake following UVB exposure and resulted in anxiety-related behaviors, suggesting that p53 plays a role in appetite stimulation and anxiety via UVB-induced β-endorphin production.

This study investigated novel genetic tools to manipulate hair follicle compartments in mice and found that altering dermal papilla genes can significantly impact hair pigmentation.

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.

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.

This study suggests that ovarian cycle-related progesterone and neurosteroids regulate α2-subunit expression of GABA-A receptors in the hippocampus through a pathway independent of progesterone receptors, potentially affecting brain conditions linked to the menstrual cycle.

In this study, researchers observed that the absence of the vitamin D receptor or its ligand-activated transcription in mice did not affect glucose homeostasis or gene expression in islets.

This review discusses the roles of androgens and androgen receptors in skin-related disorders and suggests that targeting androgen receptors may be a more effective treatment strategy.

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 CD34 is necessary for TPA-induced activation of hair follicle stem cells and tumor formation in mice, with CD34 knockout mice showing delayed and reduced tumor development compared to wild-types.

This study found that Dab2 conditional knockout mice experienced delayed hair follicle cycles and reduced hair follicle stem cell activity, suggesting Dab2's crucial role in regulating stem cell activation and anti-aging process in hair follicles.

This study found that FRβ knockout mice exhibited autoimmune symptoms and slower tumor growth compared to wild type mice, suggesting that the FRβ receptor may play a role in regulating immune responses in tumors and autoimmune conditions.

This study found that administering calcium blockers verapamil or nimodipine significantly preserved auditory function and hair cell survival in Cx26-cKO mice, suggesting potential protective effects for other inner ear disorders.

This study found that vitamin D regulation plays a crucial role in connecting metabolic and cardiovascular conditions, influencing gene expression related to these disorders in both kidney and heart tissues.

Loss of Dsc3 function in the epidermis impaired cell adhesion, leading to blistering and hair loss, which suggests a potential cause of PV-like skin diseases according to this study.

This study observed that PCR-based genotyping for cre-loxP mice can lead to errors due to cre-mediated recombination in non-target tissues like tails, affecting the detection of lox alleles.

This study found that the retinol dehydrogenases SDR16C5 and SDR16C6 in mice play a crucial role in skin retinol dehydrogenase activity, affecting hair growth and gland functions without impacting survival.

Estrogen receptor α controls hair growth cycles and skin thickness in male mice.