314 citations
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April 2010 in “Developmental Cell” β-catenin in the dermal papilla is crucial for normal hair growth and repair.
7 citations
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August 2017 in “European journal of endocrinology” Mutations in the POC1A gene can cause a unique form of extreme insulin resistance and short stature.
1 citations
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October 1988 in “Clinics in Dermatology” Scientists identified and cloned specific keratin proteins in mouse hair.
6 citations
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September 2015 in “Journal of Investigative Dermatology” Using special RNA to target a mutant gene fixed hair problems in mice.
29 citations
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July 2014 in “PloS one” Meis1 is crucial for skin health and tumor development.
July 2002 in “Science s STKE” Modified β-catenin causes different effects in hair and skin cells, leading to cysts or tumors.
45 citations
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January 2010 in “Journal of Veterinary Medical Science” A gene mutation causes curly hair and hair loss in rats.
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.
20 citations
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July 2005 in “Experimental dermatology” The fuzzy gene is crucial for controlling hair growth cycles.
January 1999 in “American Journal of Medical Genetics Part A” The report expanded knowledge of MBTPS1-related disorders by identifying new symptoms.
2 citations
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May 2023 in “Veterinary Pathology” Understanding genetic variations in mice is crucial for studying skin, hair, or nail abnormalities.
July 2017 in “Cancer Research” Krt15+ cells in mice can resist radiation, regenerate tissue, and start tumors, suggesting new cancer treatment targets.
February 2024 in “bioRxiv (Cold Spring Harbor Laboratory)” Increased energy use in Pik3r1-related insulin resistance isn't due to Ucp1 thermogenesis.
88 citations
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August 1998 in “Carcinogenesis” High levels of ODC and a mutant Ha-ras gene cause tumors in mice.
48 citations
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April 2008 in “Human Molecular Genetics” Progerin affects cell shape but not hair or skin in mice.
12 citations
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January 1987 in “Carcinogenesis” TCDD changes skin cell growth and keratin production in mice.
14 citations
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March 1995 in “Journal of cell science” SV40 T antigen in hair follicles causes abnormal hair and health issues in mice.
10 citations
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April 2008 in “Journal of Pediatric Surgery” P-selectin is not the only factor that prevents scarring in fetal wound healing in mice.
3 citations
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March 2023 in “Annals of the New York Academy of Sciences” Mutations in claudin-1 and claudin-3 cause hair loss in baby mice.
62 citations
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December 1966 in “Endocrinology” Injecting α-MSH made mice's hair turn black.
December 2021 in “OPAL (Open@LaTrobe) (La Trobe University)” BBS7 is crucial for maintaining healthy periodontal ligaments by supporting Shh signaling.
9 citations
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May 2019 in “Medicine” The C-allele and CC-genotype in the PTPN22 gene lower the risk of alopecia areata.
44 citations
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March 2012 in “Molecular Carcinogenesis” Keratin 15 cells from hair follicles help develop and maintain skin tumors in mice.
81 citations
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September 2009 in “Birth defects research” Different body areas in mice produce different hair types due to interactions between skin layers.
1 citations
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April 2024 in “Metabolites” Activated protein C helps protect mice from long-term radiation damage.
17 citations
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June 2011 in “The journal of investigative dermatology/Journal of investigative dermatology” The G60S Connexin43 mutation causes hair growth issues and poor hair quality in mice, similar to human ODDD patients.
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.
April 2024 in “bioRxiv (Cold Spring Harbor Laboratory)” Removing Sprouty genes in mice causes various hormone-related issues but does not increase cancer risk by one year of age.
May 2024 in “Animal genetics” A cat's poor wound healing was linked to a genetic deletion in the COL5A1 gene.
3 citations
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December 2020 in “Scientific reports” Mitochondrial problems in tooth cells lead to bad enamel and dentin development in mice.