Deleting the MAD2L1 gene is tolerated in certain mouse cancer models.
1 citations
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April 2010 in “Digital WPI” CLK1 is needed for skin cells to become epidermal cells but not sebocytes.
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January 2019 in “Aging” Lack of functional CYLD in mice leads to early aging and cancer.
August 2001 in “The Journal of Cell Biology” A new keratin gene was found in mice, explaining hair growth.
April 2018 in “Journal of Investigative Dermatology” CREB, a protein that can promote cancer traits, is controlled by β-catenin in skin cancer cells.
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.
April 2018 in “Journal of Investigative Dermatology” CENPV, a new partner of CYLD, helps regulate ciliary acetylated tubulin and is overexpressed in certain skin tumors.
53 citations
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August 2005 in “The Journal of Cell Biology” Sgk3 is essential for normal hair follicle growth and maintenance.
April 2023 in “Journal of Investigative Dermatology” Blocking casein kinase 1 in skin cells can help melanocyte precursors move better, potentially helping with conditions like vitiligo or gray hair.
99 citations
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February 2000 in “PubMed” Overexpressing PKCepsilon in mice reduces papillomas but increases carcinomas.
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October 2003 in “Genetics” The mK6irs1/Krt2-6g gene likely causes wavy hair in mice.
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November 2022 in “Cell Death and Disease” CEP135 may predict cancer outcomes, and targeting PLK1 could help treat certain sarcomas.
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June 2015 in “Journal of Investigative Dermatology” aPKCλ is crucial for keeping hair follicle stem cells inactive and maintaining normal hair growth.
48 citations
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October 2004 in “Molecular and Cellular Biology” Mice with a specific BRCA1 mutation have a higher risk of tumors, especially in the uterus and ovaries.
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December 2016 in “The EMBO Journal” Gata6 is important for protecting hair growth cells from DNA damage and keeping normal hair growth.
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February 2003 in “American Journal of Medical Genetics Part A” A chromosomal change may cause ectodermal dysplasia and developmental issues in a child.
March 2007 in “Journal of Cell Science” K10 may not prevent tumors as previously thought and might increase benign tumor risk.
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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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November 2011 in “The Journal of Dermatology” Connexin-26 gene mutations may increase cancer risk in KID syndrome patients.
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December 2011 in “Journal of Biological Chemistry” p63 is essential for skin cell growth and differentiation by controlling specific gene networks.
August 2012 in “Nature Cell Biology” The tumor suppressor BRCA2 helps in cell division by bringing key proteins to the area where cells split.
September 2016 in “Journal of Dermatological Science” The protein aPKCλ is crucial for keeping hair follicle stem cells inactive and for hair growth and regeneration.
April 2023 in “Journal of Investigative Dermatology” ALRN-6924 can protect hair follicles from chemotherapy damage by temporarily stopping cell division.
1 citations
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April 2012 in “Cancer Research” Antizyme reduces tumor growth and normalizes skin cell development affected by MEK.
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February 2019 in “Experimental & Molecular Medicine” PAK4 is crucial in cancer progression, brain development, and could be a therapeutic target, especially through the PAK4-CREB axis.
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February 2006 in “Cancer Research” Patched1 helps prevent tumors by controlling cell growth.
139 citations
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December 1998 in “The journal of investigative dermatology/Journal of investigative dermatology” K6hf is a unique protein found only in a specific layer of hair follicles.
January 2025 in “Cell Communication and Signaling” CXXC5 can both suppress and promote cancer, making it a complex target for treatment.
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May 2008 in “Journal of Clinical Oncology” AZD6244 treatment causes skin aging effects by depleting skin stem cells.
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February 2001 in “Journal of Dermatological Science” p21waf1/cip1 and p27kip1 help in hair follicle differentiation in rats.