|Application ||WB, IHC|
|Calculated MW||53704 Da|
|Other Names||Keratin, type II cytoskeletal 8, Cytokeratin-8, CK-8, Keratin-8, K8, Type-II keratin Kb8, KRT8, CYK8|
|Target/Specificity||A synthetic pathway corresponding to residues on the C-terminus of human CK8 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-8 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Together with KRT19, helps to link the contractile apparatus to dystrophin at the costameres of striated muscle.|
|Cellular Location||Cytoplasm. Nucleus, nucleoplasm Nucleus matrix|
|Tissue Location||Observed in muscle fibers accumulating in the costameres of myoplasm at the sarcolemma membrane in structures that contain dystrophin and spectrin. Expressed in gingival mucosa and hard palate of the oral cavity.|
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Provided below are standard protocols that you may find useful for product applications.
Keratins, the intermediate filament proteins of epithelial cells, connect to desmosomes, the cell-cell adhesion structures at the surface membrane. Among the various intermediate filament (IF) proteins, cytokeratin 8 (CK8) is especially remarkable as it is produced early in embryogenesis, is the only type-II CK occurring in many simple epithelial cells, and can also be synthesized in certain non-epithelial cells (1). Keratin 8 and 18 (CK8/18) are the major keratin pair in simple-type epithelia, as found in the liver, pancreas, and intestine (2). While K8/K18 are essential for maintaining structural integrity, there is accumulating evidence indicating that they also exert non-mechanical functions. It has been reported that K8/K18-free hepatocytes from K8-null mice are more sensitive to Fas-mediated apoptosis, in line with an increased Fas density at the cell surface and an altered c-Flip regulation of the anti-apoptotic ERK1/2 signaling pathway (3).
1. Krauss S, et al. Gene 86(2):241-9, 1990
2. Ku, NO, et al. J. Clin Invest 99(1):19-23, 1997.
3. Galarneau L, et al. Exp Cell Res. 313(1):179-94, 2007
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