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Arch Dermatol. 2001;137:1236-1238.

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DURING THE past decade, our understanding of the role of keratins in ectodermal structures has led to the discovery of the molecular bases of several genetic disorders of skin (for reviews, see Irvine and McLean¹ and Corden and McLean²). Keratin gene mutations in patients with epidermolysis bullosa simplex were first described in 1991, after generation of a transgenic mouse model with deletion of a critical region of keratin 14 (K14) that resembled the human phenotype of the Dowling-Meara subtype. The known localization of specific keratin gene expression in epidermis and other ectodermal sites then led to the discovery of K1 and K10 keratin gene mutations in patients with epidermolytic hyperkeratosis (EH, ichthyosis bullosa of Brocq); K2e mutations in ichthyosis bullosa of Siemens; K9 mutations in the epidermolytic (Vorner) form of palmoplantar keratoderma; K6a, K6b, K16, and K17 mutations in pachyonychia congenita; K4 and K13 . . . [Full Text of this Article]

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