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November 2019 in “Cell calcium” The STIM1 R304W mutation in mice leads to bone changes and teeth hair growth.
March 2011 in “Open Archive (Karolinska Institutet)” The mouse model showed defects in adult stem cell maintenance related to Hutchinson-Gilford progeria syndrome.
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October 2002 in “Human molecular genetics online/Human molecular genetics” A gene mutation in mice causes skin defects and early death.
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September 2017 in “Journal of Investigative Dermatology” Notch1 signaling is impaired in hidradenitis suppurativa, affecting skin and hair cells.
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November 2024 in “Blood” PI3Kδ inhibition may effectively treat cutaneous chronic graft-versus-host disease.
The microenvironment affects the behavior and survival of melanocytes with the GNAQ oncogene in melanoma.
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October 1998 in “Experimental Dermatology” Normal skin results from interactions between EGF and the Tabby mutation.
September 2022 in “bioRxiv (Cold Spring Harbor Laboratory)” The Kras mutation changes normal cell signals, leading to disrupted tissue structure and potential cancer.
May 2026 in “Scientific Reports” Overexpression of LRIG3 in skin causes hair loss.
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September 2004 in “Biomacromolecules” The Glu413Lys mutation in keratin affects hair stability, while Glu413Asp does not.
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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.
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December 2014 in “The American journal of pathology” A gene deletion in mice causes weak protein, immune issues, hair loss, airway problems, and wasting disease.
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July 2023 in “Cells” MG53 helps reduce skin damage caused by nitrogen mustard.
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September 2000 in “Journal of Biological Chemistry” GKLF/KLF4 and Sp1 control Keratin 19 gene activity, influencing cancer-related changes.
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February 2018 in “Oncotarget” Lower SMAD2/3 activation predicts more severe skin cancer.
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July 2004 in “Molecular genetics and genomics” A new mouse mutation causes skin and hair defects due to a gene change.
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January 2010 in “Human Molecular Genetics” FTase and GGTase-I are essential for skin keratinocyte health.
January 2017 in “Jikken doubutsu ihou/Jikken doubutsu/Experimental animals/Jikken Dobutsu” Mice with a changed Hr gene lose and regrow hair due to changes in the gene's activity.
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August 2008 in “The journal of investigative dermatology/Journal of investigative dermatology” TGase 3 helps build hair structure by forming strong bonds between proteins.
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May 2014 in “Journal of Biological Chemistry” A chimeric keratin partially improved skin structure in mice lacking keratin 5, but didn't fully restore normal skin.
Keratinocytes can reduce the survival of certain melanoma cells, suggesting new therapy paths.
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October 2010 in “Journal of Investigative Dermatology” Activating Kras in mouse skin causes excess skin and hair loss.
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July 2002 in “Journal of Investigative Dermatology” Desmoglein 1 can partly make up for the loss of Desmoglein 3 in hair adhesion but not in mucous membranes.
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August 2008 in “Immunogenetics” A gene mutation in mice causes increased mast cells and disorganized hair follicles in their skin.
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April 1995 in “The journal of cell biology/The Journal of cell biology” A new protein was made to detect specific skin cell growth receptors and worked in normal skin but not in skin cancer cells.
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July 2010 in “The FEBS journal” The study found a specific peptide that helps detect TGase 3 activity in skin and hair follicles.
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April 2018 in “EMBO journal” The protein SLC1A3 is important for activating skin stem cells and is necessary for normal hair and skin growth in mice.
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August 2023 in “The journal of pharmacology and experimental therapeutics/The Journal of pharmacology and experimental therapeutics” Kir6.1 mutations in Cantú syndrome increase channel sensitivity and hyperpolarization, while SUR2B mutations do not.
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November 2007 in “Genomics” Mutations in specific keratin genes cause improper hair structure in mice due to faulty keratin protein assembly.
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November 2015 in “Carcinogenesis” Deleting TNFα gene reduces skin cancer risk in certain mice.