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In this study, researchers found that deleting the Bmi1 gene in murine melanocytes caused premature hair greying and loss of melanocyte lineage cells, highlighting BMI1's role in protecting melanocyte stem cells from stress and oxidative damage.

This study found that the Foxn1(-/-) nude phenotype significantly influences epithelial progeny in skin, with notable changes in stem cell niches not achievable in other models.

In this study, researchers observed that TCDD exposure in mice enhanced sebaceous gland differentiation and lipid production before causing seboatrophy, providing insights into the cellular events that may contribute to chloracne pathogenesis.

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.

Cathepsin L deficiency causes hair and skin issues in mice.

This study found that the mutant hairless rhino bald protein in mice interacts with the vitamin D receptor but cannot repress its transactivation and shows abnormal cellular localization.

In this study, the disruption of Gh/tissue transglutaminase in mice did not affect viability but reduced thymocyte viability and fibroblast adhesion, suggesting its role in cell stabilization and extracellular matrix interactions.

This study found that overexpression of PKCα in mouse epidermis increases expression of specific proinflammatory mediators and induces inflammation but does not significantly affect epidermal differentiation, proliferation, or tumor promotion with TPA.

This study found that certain C57BL/6 mouse substrains have a genetic vulnerability to skin lesions resembling central centrifugal cicatrical alopecia in humans, potentially worsened by high vitamin A levels.

This article describes a method using the CUBIC protocol to clarify and visualize molecular and cellular interactions in mouse skin biopsies at single cell resolution, but does not provide new biological findings.

This study found that deleting the transcription factor Twist1 in keratinocytes significantly reduced UVB-induced skin carcinogenesis in mice, suggesting a potential target for preventing cutaneous squamous cell carcinoma.

This study found that the retinoid LGD1069 suppressed mammary tumorigenesis in a mouse model without observable toxicity, while TTNPB showed modest effects but was associated with significant toxicity.

In this study, early prenatal treatment with Minoxidil, a lysyl hydroxylase inhibitor, partly improved cardiac outflow tract septation in Tbx1 mutant mice, suggesting that inhibiting collagen cross-linking may mitigate some effects of Tbx1 mutation associated with DiGeorge syndrome.

This study found that mutations in the Foxn1 gene in nude mice affect not only hair but also nail structure and differentiation, offering insights into nail hypergranulosis pathogenesis relevant to human nail diseases.

The mutation causes hairless mice due to mislocalized and dysfunctional HR protein.

This study developed new immortalized keratinocyte cell lines lacking COL7A1 using CRISPR/Cas9 technology, providing a valuable model to explore the biology and treatment options for recessive dystrophic epidermolysis bullosa.

CaBP1 and CaBP2 are important for continuous hearing by preventing inactivation of calcium currents in ear cells, with CaBP2 also able to restore hearing when reintroduced.

This research observed that the skeletal abnormalities in Noggin null mice varied based on genetic background, and identified haploinsufficiency leading to joint fusions, similar to human conditions associated with NOGGIN deficiency.

In this study, researchers evaluated CS12192, a selective JAK3 inhibitor, in an alopecia areata mouse model and found it reversed hair growth inhibition comparably to baricitinib, with better safety and similar immune-modulating mechanisms.

This study found that the immune-competent B6. Cg‐Tyr c−2J Hr hr /J congenic mouse line had a more pronounced delayed sunburn response and different proliferative skin reactions to UV exposure compared to SKH 1 mice.

This study reported that heterozygosity for FHIT affects mice's susceptibility to spontaneous alopecia areata and to certain preneoplastic lesions induced by benzo[a]pyrene, but does not change how they respond to budesonide and N-acetyl-L-cysteine.

This study found that conditional expression of TGFβ1 in mice affects epidermal and hair follicle growth, with chronic expression causing severe alopecia and a negative feedback loop involving Smad7.

In this study, Brca1(S971A/S971A) mice showed a moderately increased risk of spontaneous tumor formation and defects in DNA damage response, suggesting CHK2 phosphorylation of BRCA1 is crucial for tumor suppression.

In this study, researchers found that β-catenin directly promotes TERT expression in stem and cancer cells by interacting with the Tert promoter, illustrating a mechanistic link between tumorigenesis and pluripotency.

This study found that overexpression of β-catenin in bipotent Schwann-cell precursors promotes melanocyte development in limb areas by inducing MITF and repressing FoxD3, especially during a specific developmental timeframe.

This study found that mice lacking syndecan-1 experienced cold stress and metabolic issues due to reduced intradermal fat, which was restored by thermoneutral housing or rosiglitazone treatment.

In this study, transgenic mice with a truncated latent transforming growth factor-beta-binding protein showed reduced keratinocyte proliferation and alterations in the hair cycle due to mis-localization of transforming growth factor-beta.

This study found that PK11195 treatment weakened exploratory behavior in two strains of mice, while finasteride and indomethacin decreased exploration in laboratory rodents regardless of species.

This study found that Pik3r1 Y657* mice, which model human SHORT syndrome, show increased energy expenditure despite insulin resistance, but this is not due to changes in locomotion, thermoregulation, or Ucp1-dependent thermogenesis, suggesting a different metabolic mechanism may protect against lipotoxicity.