23 citations
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August 1975 in “Experimental Biology and Medicine” Copper supplements during pregnancy improve survival and development in mutant mice.
8 citations
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April 2016 in “Experimental dermatology” B6.Cg-Tyr c−2J Hr hr /J mice have a stronger delayed sunburn reaction and are good for UV research.
1 citations
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July 2007 in “Journal of Investigative Dermatology” The mutation causes hairless mice due to mislocalized and dysfunctional HR protein.
11 citations
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June 2012 in “Acta histochemica” Mice with a Gsdma3 gene mutation have thicker skin and longer hair follicle openings due to increased β-catenin levels.
135 citations
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May 1994 in “Medical Entomology and Zoology” Mouse models help study genetic skin diseases.
Researchers made a mouse model with curly hair and hair loss by editing a gene.
1 citations
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June 2022 in “Experimental dermatology” The SHJH hr mice with a mutated Hr gene show signs of faster skin aging due to poor antioxidative protection.
February 1999 in “The anatomical record” Two mouse mutants have defective hair cuticle cross-linking.
11 citations
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January 2005 in “Brazilian Journal of Medical and Biological Research” Hairless USP mice have enlarged skin cysts as they age.
30 citations
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December 2001 in “Experimental dermatology” Gonadal hormones significantly affect the severity of alopecia areata in mice.
2 citations
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February 2023 in “Transgenic Research” The E2 protein affects gene activity in hair follicles of mice.
23 citations
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June 2003 in “Journal of Investigative Dermatology Symposium Proceedings” Alopecia Areata is an autoimmune disease affecting hair follicles, influenced by genetic and environmental factors, with rodent models being essential for research.
The balance between cell renewal and differentiation controls the growth of cancerous cells in mouse skin.
18 citations
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February 2006 in “Genomics” A new genetic mutation in mice causes permanent hair loss and skin wrinkling.
143 citations
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May 2002 in “PubMed” LGD1069 effectively prevents breast tumors in mice without toxicity.
11 citations
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November 1991 in “Journal of Neuropathology & Experimental Neurology” Brindled mice show abnormal catecholamine neuron development due to copper deficiency.
Introducing the OTC gene improved symptoms in mice with OTC deficiency.
August 2024 in “Current Protocols” The C3H/HeJ mouse model is useful for studying and testing treatments for alopecia areata.
1 citations
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January 2024 in “Animal Research and One Health” Mouse models are essential for studying and improving genetic traits in agriculture.
69 citations
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July 2002 in “Clinical and Experimental Dermatology” Alopecia areata is influenced by genetics and immune system factors, and better understanding could improve treatments.
Adenophora Radix extract can promote hair growth and increase melanin in mice.
53 citations
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October 2014 in “Free radical biology & medicine” Defective mitochondrial DNA replication causes aging symptoms and increased oxidative damage in mice.
January 2008 in “HAL (Le Centre pour la Communication Scientifique Directe)” The mutant HR bmh protein affects hair follicle formation by failing to repress vitamin D receptor activity.
Spiny mice have resilient, large mitochondria that help them regenerate tissue.
7 citations
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November 2010 in “Genesis” Mouse Scube3 affects teeth, tongue, vibrissae, and eye development, but not facial structure or limb growth.
November 2023 in “Biomolecules” The research showed that Vitamin D and its receptor are important for healthy bones and normal hair and skin in rats.
The naked mutation in mice causes hair loss and helps identify keratin genes.
20 citations
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April 2000 in “Experimental dermatology” ODC transgenic mice can model human hair loss with skin lesions.
10 citations
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November 2009 in “Pigment cell & melanoma research” The document concludes that MGRN1 affects mouse fur color by interfering with a receptor's signaling, but its full role in the body is still unknown.
August 2020 in “bioRxiv (Cold Spring Harbor Laboratory)” Normal cells outcompete and remove mutant cells in the pancreas with the help of the EphA2 receptor.