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Keratins 6, 16, and 17 (K6/K16/K17) are a group of type I and type II intermediate filament proteins that are characteristically upregulated in epithelial cells during stress, injury, and hyperproliferative states (Moll et al., 2008, PubMed: 18503443). While they provide essential mechanical support to the cytoskeleton, they also function as dynamic signaling molecules that regulate cell migration, protein synthesis, and inflammatory responses (Kim et al., 2006, PubMed: 16530047). In clinical medicine, mutations in the genes encoding these keratins lead to keratinopathies such as Pachyonychia congenita, while their overexpression is a hallmark of psoriasis and various epithelial malignancies (Leachman et al., 2010, PubMed: 20404824). Keratin 17, in particular, has been identified as a major T-cell autoantigen in psoriasis and a driver of oncogenic signaling in squamous cell carcinomas (Depianto et al., 2010, PubMed: 20351061). Therapeutic interventions targeting these keratins include gene-silencing siRNAs like TD101 and small molecules such as retinoids and vitamin D analogs that modulate their transcription (Smith et al., 2008, PubMed: 18503443). Monitoring the expression levels of these keratins serves as a valuable biomarker for disease severity in dermatology and prognosis in oncology.
RNA interference (siRNA) mediated gene silencing; Transcriptional modulation via nuclear receptors (RAR and VDR)
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