52 citations
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July 2011 in “PubMed” TRPS1 is crucial for bone, kidney, and hair follicle development.
21 citations
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August 2014 in “Journal of Cell Communication and Signaling” Tsukushi helps control inflammation and aids in wound healing.
January 2022 in “bioRxiv (Cold Spring Harbor Laboratory)” The gp130 receptor helps in tissue regeneration and disease progression, and manipulating it could improve healing and prevent disease.
489 citations
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November 2021 in “Signal Transduction and Targeted Therapy” The JAK/STAT pathway is important in cell processes and disease, and JAK inhibitors are promising for treating related conditions.
14 citations
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July 2021 in “Bioscience Reports” Activating Tgr5 may help treat hair loss and bone loss.
November 2023 in “Advanced Science” A specific hair protein variant increases the spread of breast cancer and is linked to worse survival rates.
46 citations
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November 2007 in “Gene Expression Patterns” Trps1 plays a key role in hair follicle development and cycling.
14 citations
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November 2024 in “International Journal of Molecular Sciences” YAP and TAZ proteins control skin cell growth and repair.
May 2006 in “The Journal of Cell Biology” Keratin 17 is crucial for cell growth in wound healing by aiding protein synthesis.
April 2016 in “Journal of Investigative Dermatology” Decreasing MIG6 can increase the movement and invasiveness of MEK-inhibited mutant NRAS melanoma, particularly when stimulated by EGF.
December 2022 in “KSBB Journal” Activating TLR3 boosts autophagy gene expression in skin cells.
April 2012 in “Cancer Research” Stat3 influences keratinocyte stem cell behavior, affecting differentiation and migration.
Proper niche formation in Drosophila requires Slit-Robo signaling for cell migration.
March 2026 in “Calcified Tissue International” The EDA pathway plays a key role in bone development by interacting with other signaling pathways.
November 2025 in “Journal of Investigative Dermatology” TEDAR is crucial for skin cell differentiation and barrier formation.
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November 2019 in “Cancer reports” The Wnt signaling pathway is not a major factor in the development of keratoacanthoma, a type of skin tumor.
60 citations
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August 2008 in “Human molecular genetics online/Human molecular genetics” A position effect on the TRPS1 gene causes excessive hair growth in humans and mice.
July 2024 in “Journal of Investigative Dermatology” 11 citations
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November 2015 in “Carcinogenesis” Deleting TNFα gene reduces skin cancer risk in certain mice.
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May 1995 in “Proceedings of the National Academy of Sciences” A specific gene region can control targeted and responsive gene expression in mice, useful for skin disorder treatments.
November 2022 in “The journal of investigative dermatology/Journal of investigative dermatology” Deleting the CD271 gene in mouse skin cells leads to disorganized skin and increased hair growth, suggesting CD271 is important for skin health.
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January 2005 in “Photochemistry and Photobiology” Protein kinase C epsilon may increase skin cancer risk by affecting nearby cells.
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September 2017 in “Journal of Investigative Dermatology” TRPV3 in skin cells causes inflammation and cell death.
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October 1997 in “Nature” 3 citations
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January 2005 in “Photochemistry and Photobiology” Protein kinase C epsilon may promote skin cancer development after UV exposure by affecting nearby cells.
Skin cells can naturally limit the growth of cancerous changes by balancing cell renewal and differentiation.
73 citations
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November 2000 in “Proceedings of the National Academy of Sciences of the United States of America” There are two ways to start hair growth: one needs Stat3 and the other does not, but both need PI3K activation.
April 2017 in “Journal of Investigative Dermatology” Triptolide effectively and safely reduces actinic keratosis lesions in mice.
10 citations
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January 2013 in “Journal of skin cancer” PKC ε increases hair follicle stem cell turnover and may raise skin cancer risk.
July 2025 in “Journal of Investigative Dermatology” TGF-β signaling is essential for hair follicle regeneration during wound healing.