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This study found that progesterone's antiseizure effects in mice occurred primarily through conversion to allopregnanolone, rather than through the progesterone receptor, as evidenced by results in PR knockout mice.

In this study, the researchers found that alopecia in VDR null mice is likely due to issues with hair cycle initiation rather than defects in keratinocyte proliferation or differentiation.

TRPV1 helps regulate hair growth cycles.

This study suggests that alopecia in vitamin D receptor null mice is due to impaired initiation of the hair cycle rather than defects in keratinocyte proliferation or differentiation.

This study found that the PP2A-B55α regulatory subunit is crucial for ectodermal development in mice, with knockout embryos displaying severe neural and epidermal defects and failing to survive to birth.

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

Iron deficiency causes hair loss by affecting hair differentiation and cycling.

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 VDR knockout mice exhibited muscle and motor impairments affecting locomotor behavior, while cognitive functions such as exploration, working memory, and anxiety appeared unaffected.

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 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.

IL-1 receptor absence in mice leads to skin cysts and changes in immune response after UVB exposure.

This study found that vitamin C deficiency in SMP-30/GNL-KO mice affected gene expression related to hair growth and cell growth, resulting in delayed hair growth compared to those with adequate vitamin C.

This study found that OM-X® supplementation effectively prevented adverse biological changes caused by vitamin C deficiency in SMP30/GNL KO mice, improving energy maintenance, antioxidant capacity, and protein synthesis.

This study observed that mice with a whole-body deficiency of Cystathionine-β-synthase developed severe hyperhomocysteinemia and related mild symptoms without increased mortality, indicating HHCy may not directly cause end organ damage.

Progesterone reduces anxiety without needing progesterone receptors.

This study found that MK6a-deficient mice showed delayed reepithelialization after superficial wounding but not after full-thickness skin wounds, suggesting MK6a plays a role in activating follicular keratinocytes post-wounding.

This study observed that knocking out the 1α-hydroxylase gene in mice resulted in rickets and growth retardation, demonstrating the enzyme's crucial role in vitamin D function in animals.

This study found that maternal hephaestin knockout in mice leads to neonatal hair loss, likely due to low iron levels in the mother's milk.

This study found that alopecia in VDR-null mice persists despite undetectable vitamin D levels, indicating a defect in epithelial-mesenchymal communication due to the absence of ligand-independent receptor function.

This study found that mice lacking the Vitamin D receptor showed disrupted hair follicle cycling, which was partially restored with hedgehog signaling pathway activation, suggesting a role for this pathway in follicle regulation independent of vitamin D.

This study indicates that progesterone’s anesthetic activity in PR knockout mice is not due to progesterone receptors but is partially mediated by the neurosteroid allopregnanolone through GABAA receptor potentiation.

This study observed that Cyp27b1−/− mice exhibited growth and skeletal abnormalities similar to those of Vdr−/− mice, despite differences like the development of alopecia in Vdr−/− mice, suggesting that 1α,25D3 may directly influence chondrocyte proliferation and differentiation.

ZNF750 and MPZL3 are important in causing seborrheic dermatitis.

In this study on adult-onset, whole body Spry1/2/4 triple knockout mice, researchers observed endocrine abnormalities and no increased tumor incidence, despite similar food intake and motor function.

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.

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

This study suggests that the NCSTN knockout mouse could serve as an HS animal model, with tamoxifen potentially used for gene deletion in mice.