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This study found that mice lacking REDD1 experienced an expansion of dermal white adipose tissue through both hypertrophy and hyperplasia, suggesting a potential therapeutic target for skin adipogenesis regulation.

This study provided the first X-ray crystal structure of the mammalian steroid hormone reductase AKR1D1 and identified a disease-related mutant, P133R, which may impact bile acid metabolism and cause clinical symptoms.

In this mouse study, hair growth defects associated with the Gk5 null allele were partially alleviated by simvastatin treatment, suggesting GK5 plays a key role in skin-specific cholesterol regulation.

This study found that prolonged inhibition of DGAT1 in mice and dogs led to atrophy of sebaceous glands, with mice also experiencing alopecia, suggesting potential skin-related risks for humans using DGAT1 inhibitors.

This study found that IL-6 knockout mice exhibited increased wound-induced hair neogenesis compared to wild-type mice, likely due to enhanced STAT3 activation facilitated by compensatory cytokine activity.

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.

This study found that high levels of μ-crystallin in skeletal muscle are associated with greater fat metabolism and a shift in gene expression towards slower muscle function.

This study found that a specific mutation in the mouse RXRalpha gene significantly impacts immune responses and causes hair loss and skin cysts.

This study reports that hypomorphic alleles of the Ass1 gene in mice resemble human CTLN1, providing a potential model for preclinical studies and indicating that standard treatments for CTLN1 can rescue phenotypes.

This study observed that overexpression of Bcl-2 in certain transgenic mice accelerates catagen progression and increases hair follicle apoptosis and alopecia, while Bcl-2 deficient mice show delayed hair growth and pigmentation changes.

A new mouse mutation causes skin and hair issues, influenced by another gene.

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.

A missing mK6irs1 gene causes hair loss in mice.

This study identified a new mutation in SELH/Bc mice causing distinctive whisker and body hair abnormalities, mapped near the type I keratin cluster on chromosome 11.

In this study, mice lacking the Mcpip1 gene in their myeloid cells did not develop SCC-like tumors but instead showed increased melanocyte activity and hair loss, indicating a distinct role for myeloid Mcpip1 in skin cancer development compared to keratinocyte Mcpip1.

This study found that conditional deletion of Mof in mice resulted in severe defects in skin development, including compromised epidermal differentiation and hair growth, leading to perinatal lethality.

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.

In this study, researchers observed that mutant mice with a genetic hair loss condition exhibited significant differential expression of genes related to keratinization and hair follicle formation, providing insights into potential strategies for understanding and treating alopecia.

This study found that a mutation causing Stormorken syndrome in mice led to skeletal abnormalities and unusual hair growth, showcasing the STIM1 R304W protein’s role in bone development and cell fate.

This study observed that a CARASIL mouse model demonstrated abnormal behavior, vascular and cellular changes, and upregulation of the TGF-β/Smad signaling pathway, indicating its potential involvement in CARASIL pathogenesis.

This study reports that transgene insertion in homozygous transgenic mice causes irreversible hair loss and impaired immune function, linked to interruption of the hairless locus on Chromosome 14.

In this study, basal cell carcinoma developed in Ptch-deficient mice only after chemical treatment, not skin wounding, suggesting a second unknown event is necessary for tumor formation.

Diphencyprone initially increases mouse hair growth, then slows it, possibly due to changes in specific protein levels.

This study suggests that Foxn1 expression in keratinocytes influences pigmentation in mice, highlighting differences in the molecular mechanisms between mouse and human pigmentation processes.

This study found that activating CXCR2 on ras-transformed keratinocytes promotes migration and tumor development in a mouse skin model.

This study observed that mice lacking epidermal HSD11b1 had increased non-histaminergic itch and changes in skin nerve fibers, potentially linked to higher TSLP expression.

This study reports that overexpressing the BMP antagonist noggin in mice inhibits eyelid opening by reducing apoptosis and delaying cell differentiation in the eyelid epithelium.

This study observed that COX-2 overexpression in transgenic mice led to a significant reduction in skin tumor development compared to controls, challenging the expected role of COX-2 in promoting tumors.

In this study, knockout mice lacking the Cyp4f39 gene showed severe skin barrier dysfunction and high early mortality, suggesting its critical role in skin barrier formation and insights into ichthyosis pathogenesis.