Keratin Classes: Molecular Markers for Different Types of Epithelial Differentiation

Sequencing and automated whole-genome optical mapping of the genome of a domestic goat (Capra hircus)

“…Two types (type I and type II) of keratins are paired to form obligatory heteropolymers 34 , whereas the keratin-associated proteins may be responsible for forming the rigid hair shaft and altering the hair structure and diameter 35 . In total, we annotated 49 keratin genes (Supplementary Table 21) and 30 keratin-associated protein genes in the goat genome (Supplementary Table 22), of which 29 keratin genes and all 30 keratin-associated protein genes were detected with FPKM > 5 in both types of follicles (Supplementary Table 23).…”

Expression of Cytokeratin 14 and 19 in Process of Oral Carcinogenesis

“…However, unlike in tumors derived from glandular epithelium, the complex patterns of CK polypeptides observed in tumors arising in squamous epithelium differ from those in their tissues of origin 9) . Cytokeratins are a group of waterinsoluble proteins with a molecular weight in the range of 40-70 kD that form 8 to 11-nm intermediate filaments in a wide variety of epithelial cells 19) . These proteins are classified into two subfamilies: type I acidic (CK9-20); and type II, neutral or basic (CK1-8) 3,4,8) .…”

Molecular genetics of the skin: the implications of understanding

“…3 Subsequently defects in other components of the basement membrane and hemidesmosomes -such as laminin 332, ␣ 6 ␤ 4 integrin, collagen XVII and plectin -were shown to be responsible for other neonatal blistering disorders. 4 Similarly, the biological properties of keratin intermediate filaments were established biochemically and ultrastructurally, 5,6 but molecular genetics demonstrated that defects in specific keratins in epidermis, appendages and mucosa are responsible for a wide range of phenotypes -blistering and hyperkeratosis, pigmentary and hair defects -which reflect not only the tissue and differentiation-specific distribution of the keratins, 7 but also their nonstructural properties. Blistering and hyperkeratotic phenotypes also result from defects in cell adhesion: directly in the case of desmosomal proteins or, with endoplasmic reticulum (ER) and Golgi calcium ATPase dysfunction in Darier and Hailey-Hailey disease, via abnormal membrane protein processing.…”