Recombinant Mouse DCC Fc Chimera Protein, CF Summary
Details of Functionality
Measured by its binding ability in a functional ELISA. Immobilized rmDCC/Fc Chimera at 2 µg/mL (100 µL/well) can bind rcNetrin-1 with a linear range of 6‑400 ng/mL.
Source
Spodoptera frugiperda, Sf 21 (baculovirus)-derived mouse DCC protein
>90%, by SDS-PAGE under reducing conditions and visualized by silver stain
Endotoxin Note
<0.10 EU per 1 μg of the protein by the LAL method.
Applications/Dilutions
Dilutions
Binding Activity
Theoretical MW
146 kDa (monomer). 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
160-170 kDa, reducing conditions
Publications
Read Publications using 844-DC 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
>90%, by SDS-PAGE under reducing conditions and visualized by silver stain
Reconstitution Instructions
Reconstitute at 200 μg/mL in sterile PBS.
Notes
This product or the use of this product is covered by U.S. Patents owned by The Regents of the University of California. This product is for research use only and is not to be used for commercial purposes. Use of this product to produce products for sale or for diagnostic, therapeutic or drug discovery purposes is prohibited.
In order to obtain a license to use this product for such purposes, contact The Regents of the University of California.
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for Recombinant Mouse DCC Fc Chimera Protein, CF
Colorectal cancer suppressor
CRC18
CRCR1
DCC
deleted in colorectal cancer protein
deleted in colorectal carcinoma
IGDCC1colorectal tumor suppressor
Immunoglobulin superfamily DCC subclass member 1
immunoglobulin superfamily, DCC subclass, member 1
netrin receptor DCC
Tumor suppressor protein DCC
Background
Deleted in colorectal cancer (DCC) was originally identified as a putative tumor suppressor gene that is lost in more than 70% of colorectal cancers. This gene has also been found to be deleted in several different kinds of cancers. DCC encodes a type I transmembrane glycoprotein that belongs to the immunoglobulin (Ig) superfamily. The extracellular domain is composed of four Ig-like domains and six fibronectin type III repeats. Two forms of the protein (the long and the short isoforms) are produced from the same gene by the use of alternative initiation sites. A third isoform that is produced by alternative splicing is expressed only in the embryo. The extracellular domain of mouse DCC shares 97% and 99% amino acid sequence identity with the human and rat DCC extracellular domains, respectively. In adults, DCC is highly expressed in the brain but is also expressed at very low levels in multiple tissues. In the embryo, high levels of expression are detected in the brain and neural tube. DCC has been shown to be a receptor for the netrins that are important for axon guidance. DCC has also been shown to induce apoptosis in the absence of ligand binding and to block apoptosis when engaged by netrin-1. DCC has been shown to be a caspase substrate. The pro-apoptotic effects of DCC were found to be dependent on the proteolytic cleavage of the unoccupied receptor by caspase. It is likely that DCC functions as a tumor-suppressor gene by inducing apoptosis in cells that are not exposed to netrins.
Fearon, E.R. et al. (1990) Science 247:49.
Keino-Masu, K. et al. (1996) Cell 87:175.
Mehlen, P. et al. (1998) Nature 395:801.
Culotti, J.G. and D.C. Merz (1998) Current Opinion in Cell Biology 10:609.
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