• Purity

  >90%, by SDS-PAGE under reducing conditions and visualized by silver stain

• Endotoxin Level

  <0.10 EU per 1 μg of the protein by the LAL method.  

• Activity

  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 (Phe32 - Asn1097) Accession # P70211	DIEGRMD	Human IgG1 (Pro100 - Lys330)	6-His tag
  N-terminus			C-terminus

• Accession #

• N-terminal Sequence    
  Analysis

  Phe32

• Structure / Form

  Disulfide-linked homodimer

• Predicted Molecular Mass

  146 kDa (monomer)

• SDS-PAGE

  160-170 kDa, reducing conditions

Background: DCC

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.

• References:

1. Fearon, E.R. et al. (1990) Science 247:49.

2. Keino-Masu, K. et al. (1996) Cell 87:175.

3. Mehlen, P. et al. (1998) Nature 395:801.

4. Culotti, J.G. and D.C. Merz (1998) Current Opinion in Cell Biology 10:609.

• Long Name:

  Deleted in Colorectal Cancer

• Entrez Gene IDs:

  1630 (Human); 13176 (Mouse)

• Alternate Names:

  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