1 citations
,
August 2024 in “Transgenic Research” Activated β-catenin affects hair growth and skin thickness, and changes are reversible.
April 2021 in “The journal of investigative dermatology/Journal of investigative dermatology” CTCF protein is essential for skin and hair follicle development in mice.
7 citations
,
September 2019 in “Journal of Cellular Physiology” Akt2 protein is essential for normal cell division in early mouse embryos.
30 citations
,
February 2010 in “The journal of investigative dermatology/Journal of investigative dermatology” Plet-1 protein helps hair follicle cells move and stick to tissues.
11 citations
,
November 2015 in “Carcinogenesis” Deleting TNFα gene reduces skin cancer risk in certain mice.
2 citations
,
January 2014 in “Photochemical & photobiological sciences” Grasp protein helps maintain skin health after UVB exposure.
March 2024 in “Vestnik Rossijskogo universiteta družby narodov. Seriâ Agronomiâ i životnovodstvo” Wnt and Shh signaling are key in noggin-induced tumors, and blocking them can slow tumor growth.
Loss of the p53 gene alone causes tumors, and losing both p53 and Rb genes speeds up aggressive skin cancer.
October 2025 in “Proceedings of the National Academy of Sciences” Phospholipids help plant proteins move by regulating receptor interactions.
23 citations
,
May 2023 in “Cell Proliferation” TGF-β and FGF pathways are crucial for skin development and regeneration.
Deleting Smad4 and PTEN genes in mice causes rapid, invasive stomach cancer.
5 citations
,
November 2021 in “The journal of investigative dermatology/Journal of investigative dermatology” Wnt/β-catenin signaling is important for keeping skin cell attachment structures stable.
September 2016 in “Journal of dermatological science” TSC2 is crucial for proper hair follicle development and patterning.
44 citations
,
February 2012 in “The journal of neuroscience/The Journal of neuroscience” Mutations in the PTPRQ gene cause significant balance issues in mice due to hair bundle defects in the inner ear.
114 citations
,
July 2003 in “PubMed” Lack of KSR1 stops certain skin tumors in mice.
193 citations
,
May 2008 in “Development” Activating β-catenin can turn skin cells into hair follicles.
April 2023 in “Journal of Investigative Dermatology” Disrupting a specific protein's function in hair follicle stem cells triggers their activation and a self-healing process.
112 citations
,
January 2013 in “Experimental dermatology” Faulty Notch signalling may cause hair follicle changes and inflammation in hidradenitis suppurativa.
February 2026 in “Frontiers in Medicine” Personalized sonidegib dosing can effectively treat Gorlin-Goltz syndrome with fewer side effects.
9 citations
,
July 2022 in “Journal of Biological Chemistry” WWP2 is crucial for tooth development in mice.
52 citations
,
February 2012 in “PloS one” Lack of Ctip2 in skin cells delays wound healing and disrupts hair follicle stem cell markers in mice.
33 citations
,
June 2007 in “Gene Expression Patterns” CTIP2 may help in skin development and maintenance.
76 citations
,
June 2018 in “EMBO Reports” YAP and TAZ proteins are necessary for the development of two types of skin cancer.
3 citations
,
October 2020 in “Journal of Investigative Dermatology” Removing β-catenin in certain stem cells causes hair whitening and pigmentation issues.
January 2010 in “DukeSpace (Duke University)” Wnt and Notch pathways are crucial for repairing blood stem cells after damage.
32 citations
,
August 2016 in “Science Signaling” Alopecia areata patients show unique protein activity patterns, suggesting imbalanced signaling pathways.
26 citations
,
December 2017 in “Journal of Investigative Dermatology” Disrupting Notch signaling in blood vessels increases scarring during wound healing in mice.
September 2019 in “The journal of investigative dermatology/Journal of investigative dermatology” Tet1/2/3 enzymes affect hair follicle cell development by influencing BMP signaling.
Loss of the p53 gene alone causes tumors, and losing both p53 and Rb genes speeds up aggressive skin cancer.
January 2005 in “Enlighten: Publications (The University of Glasgow)” Melanocyte pathology requires keratinocyte hyperplasia and regulation dysfunction.