|Application ||WB, IHC|
|Calculated MW||51268 Da|
|Other Names||Keratin, type I cytoskeletal 16, Cytokeratin-16, CK-16, Keratin-16, K16, KRT16, KRT16A|
|Target/Specificity||A synthetic peptide corresponding to residues near the N-terminus of human CK-16 was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Cytokeratin-16 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Epidermis-specific type I keratin that plays a key role in skin. Acts as a regulator of innate immunity in response to skin barrier breach: required for some inflammatory checkpoint for the skin barrier maintenance.|
|Tissue Location||Expressed in the hair follicle, nail bed and in mucosal stratified squamous epithelia and, suprabasally, in oral epithelium and palmoplantar epidermis. Also found in luminal cells of sweat and mammary gland ducts|
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Provided below are standard protocols that you may find useful for product applications.
The human type I keratin 16 (CK16) is constitutively expressed in a number of complex epithelial tissues, including skin, but is better known for its induction under conditions favoring enhanced proliferation or abnormal differentiation, including wound healing, psoriasis, and cancer (1). CK16 is expressed in suprabasal interfollicular epidermis in wound healing and other pathological conditions associated with hyperproliferation, such as psoriasis and are induced when keratinocytes are cultured in vitro. However, CK16 is also constitutively expressed in normal suprabasal mucosal and palmoplantar keratinocytes (2). Pachyonychia congenita (PC) is a group of inherited ectodermal dysplasias, the characteristic phenotype being hypertrophic nail dystrophy. The PC-1 phenotype may be distinguished by the absence of the epidermal cysts found in PC-2, and it has been shown to be caused by mutations in either keratin K16 or its expression partner, the K6a isoform of K6. Mutations in K16 have also been shown to cause a milder related phenotype, focal non-epidermolytic palmoplantar keratoderma (3).
1. Paladini RD, et al. Biochem Biophys Res Commun 215(2): 517-23, 1995.
2. Shamsher MK, et al. Hum Mol Genet 4(10):1875-81, 1995
3. Smith FJ, et al. BR J Dermatol 141(6):1010-6, 1999
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