30 citations
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January 2021 in “Journal of Clinical Immunology” FOXN1 mutations can cause varying immune and physical issues, with severity influenced by gene activity and possibly other factors.
January 2009 in “China Animal Husbandry & Veterinary Medicine” The B2C promoter works in sheep cells but not in mouse embryos.
46 citations
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March 2005 in “Endocrinology” Overexpression of the glucocorticoid receptor in mice causes developmental defects similar to ectodermal dysplasia.
65 citations
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March 2004 in “Journal of Clinical Investigation” Inhibiting ornithine decarboxylase may help prevent certain skin cancers.
Knocking out the FGF5 gene in sheep increased wool production and hair-follicle density.
1 citations
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January 2022 in “Cell Biology International” Changing CDK4 levels affects the number of stem cells in mouse hair follicles.
June 2026 in “The Journal of the Kyushu Dental Society” 68 citations
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December 2010 in “The journal of investigative dermatology/Journal of investigative dermatology” HOXC13 is essential for hair and nail development by regulating Foxn1.
2 citations
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May 2022 in “Stem cell research & therapy” Disrupted stem cell signals in hairpoor mice cause hair loss.
April 2017 in “Journal of Investigative Dermatology” Researchers improved a method to study individual cells in newborn mouse skin and found a way to assess the severity of a skin condition in humans.
13 citations
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September 2019 in “Scientific Reports” High levels of the protein Flightless I worsen ulcerative colitis symptoms in mice.
10 citations
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October 2000 in “PubMed” E6/E7 oncogenes in hair follicles cause continuous hair growth by skipping the resting phase.
May 2024 in “The Journal of Immunology” Alopecia Areata can develop without perforin-mediated cytolysis.
75 citations
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October 2012 in “Journal of Investigative Dermatology” Alopecia areata can be triggered by specific immune cells without genetic or environmental factors.
3 citations
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March 2017 in “International journal of women’s dermatology” Some domesticated animals have the same genetic skin diseases as humans, which can help doctors understand human genetic mutations.
April 2023 in “The journal of investigative dermatology/Journal of investigative dermatology” A PTH-based treatment improved hair regrowth better than ruxolitinib in a mouse model of hair loss.
January 2026 in “Human Mutation” T cell subsets are crucial in kidney cancer, and a new model predicts patient outcomes using key genes.
Female rats showed more panic-related behavior than males, influenced by hormonal cycles and certain drugs.
January 2000 in “Medical Entomology and Zoology”
PTHrP is important for bone formation and may be targeted for osteoporosis treatment and longevity therapies.
26 citations
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November 2013 in “Neuroscience” Progesterone can reduce seizures without relying on the GABAA receptor pathway.
April 2023 in “Journal of Investigative Dermatology” A new image-based method improves accuracy in measuring hair loss in mice.
9 citations
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July 2022 in “Journal of Biological Chemistry” WWP2 is crucial for tooth development in mice.
3 citations
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February 2017 in “Archives of Medical Science” Finasteride treatment changes Cx43 in rat testes, possibly causing fertility issues.
25 citations
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November 2020 in “Proceedings of the National Academy of Sciences” HoxC genes are crucial for normal hair and nail development.
A rare genetic mutation causes severe immune issues, hair loss, and nail problems.
June 2025 in “Basrah Journal of veterinary Research” Vaccination and hygiene are key to preventing Feline Calicivirus in cats.
21 citations
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June 2009 in “Mammalian genome” A new mutation in the Hr gene causes hair loss in mice, similar to a human hair disorder.
131 citations
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November 1998 in “The journal of investigative dermatology/Journal of investigative dermatology” Skin grafts on mice can cause an immune response leading to hair loss, useful for studying human hair loss conditions.
113 citations
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June 2010 in “Biological Chemistry” Cathepsin L deficiency causes large, abnormal cell structures and health issues in mice.