TLDR Keratin 10 end domains may increase skin cancer risk by reducing cell death.
The study investigated the role of keratin 10 (K10) end domains in skin cancer susceptibility using K1014chim mutant mice. Contrary to expectations, these mice showed increased susceptibility to benign tumor development when exposed to a chemical skin carcinogenesis protocol, developing 2-3 times more tumors than wild-type controls. The study found that the presence of K10 end domains did not suppress keratinocyte proliferation but instead reduced apoptosis in response to environmental stressors like UV-B radiation and TNFα. This suggested that K10 end domains might interfere with apoptotic mediators, highlighting a complex role in promoting tumor growth and reducing apoptosis, which could inform future therapeutic strategies.
169 citations
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May 2006 in “Genes & Development” Keratin 17 is crucial for normal hair growth by regulating hair cycle transitions with TNFα.
92 citations
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February 2005 in “Journal of Investigative Dermatology”
70 citations
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December 2004 in “Differentiation” The study identified and characterized new keratin genes linked to hair follicles and epithelial tissues.
180 citations
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April 2002 in “Cell Death and Differentiation” 686 citations
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February 2002 in “Current Opinion in Cell Biology” Keratin filaments are crucial for cell structure and protection, with ongoing discoveries about their genes and functions.
101 citations
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August 2001 in “The Journal of Cell Biology” A new keratin 6 type in mice explains why some mice without certain keratin genes still have normal hair and nails.
149 citations
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July 2000 in “Molecular and Cellular Biology” Keratin 6a is important for quick wound healing from hair follicles.
30 citations
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October 1999 in “Differentiation” Mutant MK6a transgenes in mice cause blistering, hair loss, and potential human alopecia.
75 citations
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October 1999 in “Differentiation” Mouse keratin 6 isoforms have different expression patterns in various tissues.