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This review explores the potential benefits of non-psychoactive Cannabidiol for reducing stress and pain associated with Polycystic Ovarian Syndrome and reports no new clinical findings.

This study suggests that hairlessness in nude mice may be due to insufficient expression of phospholipase C-δ1, a molecule essential for normal hair development downstream of the Foxn1 gene.

This study identified a nonsense mutation in the Sgkl gene as the cause of defective hair growth in a mutant mouse strain, implicating the SGKL signaling pathway in hair development.

In this study, activation of c-MycER in adult mouse epidermis rapidly induced proliferation and disrupted keratinocyte differentiation, causing changes similar to precancerous lesions, which regressed once c-MycER was deactivated.

Immune cells boost stem cell activity in hairy moles, causing more hair growth.

This study found that inhibiting the Hedgehog pathway may reduce proliferation and migration in melanoma, suggesting its potential repurposing as a therapeutic target.

This study found that in Hutchinson–Gilford progeria syndrome, iPSCs committed to the keratinocyte lineage faster than normal cells, with LEF1 expression reduced and a partial rescue of the phenotype achieved through adenine base editing.

This study identified a novel G207E STING mutation causing a distinct phenotype involving alopecia, photosensitivity, and thyroid dysfunction, and suggests that common polymorphisms in TMEM173 and IFIH1 may influence disease presentation.

This study describes the first case of female pseudohermaphroditism due to a novel homozygous glucocorticoid receptor gene mutation, indicating possible pre- and postnatal virilization in affected females.

This study suggests that residues Val-889 and Arg-752 in the androgen receptor's steroid binding domain are crucial for NH2-/carboxyl-terminal interaction, affecting receptor stability and function.

This research found that activating a KrasG12D mutation in mice led to skin thickening, papillomas, and hair growth issues, suggesting that even rare KRAS mutations can mimic human RAS/MAPK syndrome symptoms.

This study found that despite carrying an activating Hras mutation, hair follicle stem cells integrate into normal skin without causing tumors, unlike similar mutations in the epidermis, suggesting unique tumor-suppressing mechanisms in hair follicles.

Keratinocyte cytokines and genetic variations influence the development of moles and skin pigmentation.

This study in engineered mouse models suggests that some basal cell carcinomas may originate from hair follicle tissue stem cells upon leaving their stem cell niche.

This study created a humanized mouse model of hereditary vitamin D-resistant rickets that lacks alopecia, indicating the mutant receptor's potential to explore the syndrome's characteristics beyond vitamin D binding.

This study found that the E6 gene, but not E7, was responsible for HPV8-induced expansion of keratinocyte stem cells in hair follicle junctional zones in mice.

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.

This study found that a novel IKZF1 mutation, p.L188V, is linked to juvenile-onset systemic lupus erythematosus and alters B-cell activation by disrupting normal DNA binding.

In this study, researchers discovered that the HrasG12V oncogenic mutation in murine skin epithelial cells initially promotes progenitor cell renewal but later leads to a balanced differentiation, stabilizing clone growth.

In this study, researchers using QM/MM simulations identified key molecular motions and residue interactions in the enzyme SRD5A2 that significantly influence its catalytic efficiency, demonstrating that specific residues play critical roles in stabilizing transition states and reducing activation barriers.

This study found that stabilized beta-catenin is crucial for activating stem cell transition from quiescence to proliferation in hair follicles by influencing gene expression within the stem cell niche.

This review discusses how chronic inflammation can lead to persistent stem cell activation and DNA damage, ultimately promoting cancer development and metastasis, but reports no new results.

This study found that the hairless gene product (Hr) suppresses VDR-mediated gene activation by directly interacting with the vitamin D receptor, potentially affecting hair follicle function.

This study found that using a novel dissolving microneedle with valproic acid effectively enhances hair follicle regrowth through improved delivery and activation of the Wnt/β-catenin pathway compared to topical application.

This study found that in a mouse model of Gorlin syndrome, constitutive activation of signaling in dermal cells led to abnormal follicular growth, indicating non-epidermal factors may contribute to the disease.

This study found that using human induced pluripotent stem cells (iPSC) carrying the causal mutation of Epidermolysis Bullosa simplex provides a robust model for understanding its molecular mechanisms and testing potential therapeutic targets.

This study discusses the involvement of Hedgehog signaling in various human cancers, detailing different mechanisms of pathway activation and highlighting the potential for therapeutic targeting through pathway inhibition.

In this study, retinoic acid treatments induced glandular and feather formation in embryos by altering positional values and activating specific retinoic acid nuclear receptor gene expression.

This study demonstrates that mice with ectopic expression of the human GLI-1 gene in their skin developed tumors resembling human basal cell carcinoma, suggesting that GLI-1 is central to tumor development without additional p53 or Ha ras mutations.

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.