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This study found that GNAQQ209L expression in mouse melanocytes led to reduced survival in the interfollicular epidermis due to paracrine signaling, while GNAQQ209L boosted survival in a different microenvironment.

This study found that mutations in type I IRS keratin genes disrupt keratin protein complexes in mice, suggesting crucial roles for these genes in proper hair coat formation.

This study found that oral biotin supplementation improved outcomes in a mouse model of inflammatory bowel disease by reducing inflammatory cytokine production and enhancing intestinal barrier integrity, suggesting potential therapeutic benefits for IBD patients.

This study reported that a Megsin-Cre transgene enables genetic manipulation primarily in skin, forestomach, and esophagus tissues, offering a new tool for studying development and diseases in these areas.

Finasteride reduces certain behaviors caused by D1-like receptor agonists but not by D2-like receptor agonists in mice.

This study found that extracellular Granzyme B contributes to skin aging and impaired healing in ApoE knockout mice by degrading essential extracellular matrix components like decorin and fibronectin.

In a study conducted on mice, researchers observed that exposure to ionizing radiation led to significant metabolic imbalances, including dyslipidemia and disruptions in amino acid metabolism, with activated protein C providing partial protection by normalizing certain plasma metabolites and lipids.

This study observed that 25-hydroxyvitamin D3 restored rickets symptoms in genetically modified rats, suggesting its direct action through vitamin D receptor pathways.

In this study, deleting the Igf1 receptor in specific skin cells of mice affected hair follicle cycling but not overall skin health, suggesting Igf1r's role in hair cycle regulation through Bmp-4 activation.

The Dfl mutation in mice causes poor sebaceous gland function and complete hair loss.

This study found that selective deletion of PIKFyve kinase using a PF4 promoter in mice led to defective platelet lysosome biogenesis and a prothrombotic effect, with unexpected macrophage infiltration in multiple organs.

This study identified a critical NF-κB-LHX2-TGFβ2 signaling pathway essential for primary hair follicle development in mice, revealing new insights into the underlying mechanisms of morphogenesis.

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.

This study suggests that inhibiting PKC, similar to rapamycin treatment, can extend lifespan and reduce neurological symptoms and inflammation in mice with mitochondrial dysfunction, potentially involving the mTORC2 pathway.

This study found that deleting the Mof gene in mouse skin leads to severe defects in skin cell self-renewal, differentiation, and hair follicle growth, indicating that MOF is crucial for mitochondrial and ciliary gene expression and essential for skin development.

In this study, the researchers reported that altering β-catenin signaling in a transgenic mouse model led to changes in skin cell fate, notably converting hair follicle cells into epidermal cells and forming cysts instead of follicles.

This study presents the G4 transgenic mouse model, which suggests a direct link between polycystic ovary syndrome and the Gm10800 gene, offering a valuable tool for understanding the disease and testing treatments.

This study demonstrates that Rac1 activity is essential for normal hair follicle formation but influences hair structure and pigmentation, in terminal differentiation, through alterations in hair shaft, cuticle, and pigmentation organization.

This study identified NM_026333 as a potential anti-aging gene that, when induced, may alleviate proton-induced aging symptoms in CF6-overexpressing and high salt-fed mice.

This study identified a single autosomal recessive gene responsible for hypotrichosis in a mutant rabbit strain, affecting hair growth and causing epidermal and hair follicle abnormalities.

This study found that in mouse pancreatic β-cells, the disruption of keratin filaments due to a specific mutation in keratin 18 resulted in altered GLUT2 localization, with less GLUT2 present on the plasma membrane compared to cells with normal keratin.

This study found that overexpression of PKCepsilon in transgenic mice reduced papilloma development but accelerated carcinoma formation in a skin tumor promotion model.

The study suggests that integrin β1 is crucial for maintaining liver microstructure and its absence may promote fibrosis by disrupting hepatocyte-extracellular matrix interactions and increasing TGF-β secretion.

This study found that aged C57BL/6 mice sub-strains exhibit distinct aging patterns, including differences in survival rates, body weight changes, and disease incidences, providing valuable insights for geriatric research using these mice models.

This study examined the expression of fatty acid transporters and binding proteins in mouse sebaceous glands and found that CD36 did not affect the localization of other related molecules.

In this study, researchers found that the loss of SETDB1 in epidermal keratinocytes led to altered chromatin states, increased ERV expression, and activation of immune responses, while inhibiting these effects with certain antiviral drugs reduced skin inflammation and hair loss in a mouse model.

In this study, researchers developed a new photoactivatable Cre recombinase mouse model, DiLiCre, which allows precise light-induced genetic modifications and cell tracing, demonstrating its effectiveness for advancing biological and biomedical research.

This study found that RXRα plays a critical role in hair cycling and keratinocyte functions in mice, likely through its interaction with VDR in epidermal cells.