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This study found that expression of certain mutant keratin genes in mice led to severe alopecia, suggesting a similar mechanism could cause hair loss in humans.

This study found that transgenic mice expressing a mutant CYLD protein lacking deubiquitinase function showed signs of premature aging and spontaneous tumor development, likely due to over-activation of specific molecular pathways and chronic inflammation.

This study suggests that the C-terminal of AHF is crucial for its binding to keratin bundles and modulating the keratin meshwork in hair follicles.

This study found that transient activation of c-Myc in transgenic mice stimulates keratinocyte proliferation and sebocyte differentiation, affecting normal epidermal and hair follicle development.

This study suggests that Mcl-1 has a non-apoptotic role in promoting keratinocyte proliferation and Wnt/β-catenin signaling, potentially indicating a novel oncogenic activity.