Recombinant Human PTK7/CCK4 Fc Chimera (Catalog # 9799-TK) binds to Recombinant Biotinylated Mouse Wnt-3a (Catalog # BT1324) with an ED50 of 4‑20 μg/mL.
Recombinant Human PTK7/CCK4 Fc Chimera Protein, CF Summary
Details of Functionality
Measured by its binding ability in a functional ELISA. In a 100 µL reaction mixture containing biotinylated Recombinant Mouse
Wnt-3a
(Catalog #
BT1324)
at 50 ng/mL and
Recombinant
Human PTK7/CCK4 Chimera
dilutions, the concentration of Recombinant Human PTK7/CCK4 Fc Chimera
that produces 50% of the maximal binding response is 4-20 μg/mL.
Source
Human embryonic kidney cell, HEK293-derived human PTK7/CCK4 protein
Human PTK7/CCK4 (Met1-Thr704) Accession # Q13308-1
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Endotoxin Note
<0.10 EU per 1 μg of the protein by the LAL method.
Applications/Dilutions
Dilutions
Bioactivity
Theoretical MW
101 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
SDS-PAGE
111-129 kDa, reducing conditions
Publications
Read Publication using 9799-TK in the following applications:
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
3 months, -20 to -70 °C under sterile conditions after reconstitution.
Buffer
Lyophilized from a 0.2 μm filtered solution in PBS.
Purity
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Reconstitution Instructions
Reconstitute at 500 μg/mL in PBS.
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for Recombinant Human PTK7/CCK4 Fc Chimera Protein, CF
CCK4
CCK-4
CCK4Colon carcinoma kinase 4
colon carcinoma kinase-4
Protein-tyrosine kinase 7
Pseudo tyrosine kinase receptor 7
PTK7 protein tyrosine kinase 7
PTK7
Tyrosine-protein kinase-like 7
Background
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).
Shin, W. et al. (2008) Biochem. Bioph. Res. Co. 371:793.
Meng, L. et al. (2010) PLoS ONE 5:e14018.
Golubkov, V. et al. (2010) J. Biol. Chem. 285:35740.
Berger, H. et al. (2017) Front. Cell Dev. Biol. 5:doi:10.3389/fcell.2017.00031.
Park, S. et al. (1996) J. Biochem. 119:235.
Golubkov, V. et al. (2014) J. Biol. Chem. 289:24238.
Prebet, T. et al. (2010) Blood. 116:2315.
Peradziryi, H. et al. (2012) Arch. Biochem. Biophys. 524:71.
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