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Keratin, type I cytoskeletal 17 (KRT17), is a member of the type I intermediate filament family primarily involved in forming structural networks in epithelial cells of hair follicles, nails, sebaceous glands, and skin appendages. It partners with keratin 6b to assemble intermediate filaments that provide mechanical resilience and protect tissues from damage. Beyond its cytoskeletal role, KRT17 is involved in wound healing, nuclear morphology regulation, gene expression, RNA processing, and cell proliferation. KRT17 expression is induced in stress and injury, and is upregulated in many cancers—with high expression correlating to tumor aggressiveness and poor outcomes. Mutations in KRT17 cause rare genetic conditions affecting nails, skin, and sebaceous glands, such as pachyonychia congenita and steatocystoma multiplex[1][2][3][4][5][6].
Not established as a therapeutic target; however, altered KRT17 expression can regulate cancer cell proliferation, migration, and chemotherapy sensitivity via modulation of signaling pathways (e.g., mTOR signaling, TNFα pathway)
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