Recombinant Human PTK7/CCK4 Fc Chimera Protein, CF

Recombinant Human PTK7/CCK4 Fc Chimera Protein, CF Summary

Product Specifications

Carrier Free

CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.

In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.

Background: PTK7/CCK4

Protein tyrosine kinase 7 (PTK7), also known as colon carcinoma kinase 4 (CCK4), is a member of the receptor tyrosine kinase superfamily (1, 2). Human PTK7 is a 1040 amino acid (aa) glycoprotein containing a 674 aa extracellular domain (ECD), a 21 aa transmembrane domain, and a 345 aa cytoplasmic tyrosine kinase homology domain. Due to the lack of the residues required for catalytic activity in the kinase domain, PTK7 is considered a pseudokinase (1, 3). The mature ECD of PTK7 contains 7 Ig-like C2 type loops and shares 92% and 91% aa identity with mouse and rat PTK7 ECD, respectively (1-4). PTK7 is expressed in a wide array of tissue types ranging from lung and liver to kidney and placenta, and has been linked to a broad range of functions (5). While originally identified as being over-expressed in colon carcinomas, PTK7 has been shown to play a role in embryogenesis, epithelial tissue organization, angiogenesis, cell motility, and survival (1, 6, 7). PTK7 has been shown to be an important regulator of the Wnt signaling pathways, both canonical and non-canonical, and is linked to the regulation of the planar cell polarity pathway (3, 6). Soluble forms of PTK7 are known to be shed from the cell surface by matrix metalloproteinases (MMPs), a disintegrin domain and metalloproteinases (ADAMs), and gamma -secretase (3, 6). The soluble form is a co-receptor for the Semaphorin/Plexin and VEGF signaling pathways (8). Deregulation of PTK7 signaling has now been observed in numerous cancers including colon, gastric, lung, and acute myeloid leukemia (1, 3). Recent studies have shown that PTK7 expression promoted increased migration and resistance to apoptosis in leukemic cells and acute myeloid leukemia (AML) blasts, while knock-down of PTK7 induced apoptosis in colorectal carcinoma cells (2, 7). Further, other studies have suggested that the ratio of full-length vs. cleaved protein, not just expression, contributes to PTK7's metastatic effects in cancer (6).

Related Research Areas

• Cancer Biomarkers
• Receptor Tyrosine Kinases (RTKs)
• Receptor Tyrosine Kinases (RTKs) in the Akt Pathway
• Wnt Receptors