188 citations
,
June 1998 in “Molecular cell” Researchers created a mouse with the same mutation as humans with trichothiodystrophy, showing similar symptoms and confirming the condition is due to defects in DNA repair and gene activity.
1 citations
,
October 2019 in “PubMed” Removing the p75 gene in mouse skin cells didn't affect their skin or hair growth.
Deleting Smad4 and PTEN genes in mice causes rapid, invasive stomach cancer.
88 citations
,
August 1998 in “Carcinogenesis” High levels of ODC and a mutant Ha-ras gene cause tumors in mice.
2 citations
,
January 2023 in “Frontiers in Genetics” Overexpressing ovine β-catenin in mice skin increases hair follicle density and growth.
Lack of certain cells causes abnormal nipple development and nursing failure.
August 2024 in “Current Protocols” The C3H/HeJ mouse model is useful for studying and testing treatments for alopecia areata.
12 citations
,
February 2017 in “Journal of neuroscience research” Removing certain brain receptors in mice worsens seizure severity and response to treatment during hormone withdrawal.
31 citations
,
November 2015 in “PloS one” Reducing Tyrosinase prevents mature color pigment cells from forming in mouse hair.
January 2025 in “SSRN Electronic Journal” 14 citations
,
February 1991 in “FEBS Letters” Introducing the rat OTC gene partially corrected OTC deficiency in mice.
6 citations
,
March 2007 in “BioTechniques” PCR genotyping in cre-loxP mice can be inaccurate due to unintended gene deletions in non-target tissues.
14 citations
,
January 2015 in “Hormones and Cancer” Androgen receptor inactivation delays skin cancer onset and reduces incidence in mice, with gender differences in susceptibility.
53 citations
,
January 1986 in “Endocrinology” Blocking a specific enzyme in male rat fetuses leads to the development of nipples and feminized genitalia.
178 citations
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June 1994 in “Journal of Investigative Dermatology” Alopecia areata in these mice is inherited, more common in young females, and can be treated with triamcinolone acetonide.
54 citations
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February 2002 in “Carcinogenesis” Increasing SSAT makes skin more prone to cancer.
April 1981 in “Pediatric research” Copper treatments increase copper in all tissues, but brindled female mice accumulate much more copper in their kidneys without clinical effects, unlike brindled male mice where brain copper deficiency is clinically significant.
15 citations
,
December 2014 in “PLoS ONE” A mutation in the iRhom2 gene causes hairless mice due to abnormal hair follicle development.
47 citations
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November 2012 in “Wound repair and regeneration” Nude mice with grafted human skin developed scars similar to human hypertrophic scars.
6 citations
,
July 1994 in “Journal of Dermatological Science” Introducing the rat OTC gene normalized hair growth in SPF-ASH mice.
May 2010 in “OPAL (Open@LaTrobe) (La Trobe University)” Vaccines and targeting TrxR variants can help prevent cancer and reduce metastasis.
56 citations
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July 2014 in “PloS one” SARMs may be an effective treatment for a certain type of breast cancer by blocking cancer growth and spread.
July 2026 in “Journal of Drug Delivery Science and Technology”
Deleting Smad4 and PTEN genes in mice causes rapid, invasive forestomach cancer.
19 citations
,
January 2015 in “Development” Hoxc8 gene helps start mammary gland development by controlling specific signals.
November 2023 in “The journal of investigative dermatology/Journal of investigative dermatology” The study developed a mouse model for Alopecia Areata that responds to treatment, useful for future research.
21 citations
,
November 2010 in “Journal of molecular medicine” FoxN1 gene is essential for proper thymus structure and preventing hair loss.
April 2022 in “Medical Molecular Morphology” 1 citations
,
April 2008 in “Pigment Cell & Melanoma Research” Foxn1 is essential for hair pigmentation by directing pigment transfer to hair cells.
2 citations
,
October 2018 in “Archives of Dermatological Research” Tofacitinib helps mice grow more hair by increasing noggin and BMP4 levels, possibly better than minoxidil.