81 citations
,
January 2006 in “Journal of cellular physiology” Mice without the vitamin D receptor gene lose hair due to disrupted hair follicle cycles.
10 citations
,
August 2013 in “Experimental Dermatology” Hairless protein and putrescine regulate each other, affecting hair growth and skin balance.
3 citations
,
April 2022 in “Frontiers in Physiology” Ptch2 plays a key role in controlling stem cell function and the ability to regenerate after birth.
24 citations
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December 2013 in “Archives of Dermatological Research” 18 citations
,
December 2016 in “European journal of pharmacology” A new compound slows cancer cell growth and causes cell death by blocking cell cycle progression and increasing cell-damaging molecules.
22 citations
,
April 2004 in “Journal of Neurochemistry” Acute stress increases Y1 receptor gene expression in certain brain areas, but repeated stress does not.
7 citations
,
January 2019 in “PeerJ” A protein called sFRP4 can slow down hair regrowth.
29 citations
,
December 2016 in “The EMBO Journal” Gata6 is important for protecting hair growth cells from DNA damage and keeping normal hair growth.
15 citations
,
December 2014 in “PLoS ONE” A mutation in the iRhom2 gene causes hairless mice due to abnormal hair follicle development.
March 2011 in “Pigment Cell & Melanoma Research” The Agouti gene influences pigmentation and may have a developmental role in deer mice.
14 citations
,
March 2015 in “Stem Cell Research & Therapy” ABCG2 protein marks stem-like skin cells in human epidermis.
4 citations
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September 2010 in “Journal of Dermatological Science” A new gene location for Keratosis follicularis squamosa was found on chromosome 7p14.3-7p12.1.
43 citations
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April 1996 in “Journal of Investigative Dermatology” 1 citations
,
September 2020 in “Journal of dermatology” Researchers found a new mutation in the LIPH gene of a woman with a rare hair condition.
The trichohyalin gene is located at chromosomal region 1q21 with other skin-related protein genes.
15 citations
,
April 2016 in “Hormones” Mutations in the NR3C1 gene cause a rare condition that affects hormone signaling and can lead to various symptoms, with dexamethasone as a treatment option.
6 citations
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April 2023 in “Current Issues in Molecular Biology” A specific gene variant may increase the risk of developing Alopecia Areata.
28 citations
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July 1993 in “The journal of investigative dermatology/Journal of investigative dermatology” September 1999 in “Molecular Carcinogenesis” Increased ODC expression makes normally tumor-resistant mice more prone to tumor development.
July 1995 in “Journal of Dermatological Science” 66 citations
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June 2004 in “Development” FGF signaling is crucial for starting feather development in chicken embryos.
4 citations
,
July 2020 in “Biochemical and Biophysical Research Communications” A protein called ectodysplasin-A2 increases a hair growth inhibitor in balding cells, which could be a target for hair loss treatment.
May 2022 in “Frontiers in Cell and Developmental Biology” miR-29a-5p prevents the formation of early hair structures by targeting a gene important for hair growth and is regulated by a complex network involving lncRNA627.1.
74 citations
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January 2006 in “The journal of investigative dermatology/Journal of investigative dermatology” Mutations in the DSG4 gene can cause a rare hair disorder similar to monilethrix.
April 2023 in “The journal of investigative dermatology/Journal of investigative dermatology” The TRPV3 channel structure changes linked to severe itch and hyperkeratosis were identified using cryo-EM.
April 2023 in “Journal of Investigative Dermatology” TGFβ-2 may cause hair loss in androgenetic alopecia.
107 citations
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June 1997 in “PubMed” EGFR is essential for normal hair development and follicle differentiation.
5 citations
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December 2018 in “Frontiers in Endocrinology” Differences in androgen receptor expression and tissue properties may lead to higher cryptorchidism risk in certain rats.
13 citations
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November 2009 in “Journal of Dermatological Science” A gene mutation causes woolly hair in a Syrian patient.