Anti-DCC

0.5mg/ml if reconstituted with 0.2ml sterile DI water. Deleted in Colorectal Carcinoma is also known as CRC18 or CRCR1. The gene encodes a functional receptor for netrin and mediates axon outgrowth and the steering response. Heterozygous loss-of-function mutations in the gene can result in congenital mirror movements. Alterations in DCC occur frequently in colorectal cancer. Studying a YAC contig containing the entire DCC coding region, they showed that the gene spans approximately 1.4 Mb. Vogelstein(1995) stated that the precise location of the gene was thought to be 18q21.3. DCC is a receptor or a component of a receptor that mediates the effects of netrin-1 on commissural axons, and they complement genetic evidence for interactions between DCC and netrin homologs in C. The protein can be detected in varying abundance in all specimens of normal colonic mucosa analyzed as well as in all specimens of adenomatous polyps, colorectal carcinoma and colorectal liver metastases. It may function as a tumor-suppressor protein by inducing apoptosis in settings in which ligand is unavailable (for example, during metastasis or tumor growth beyond local blood supply) through functional caspase cascades by a mechanism that requires cleavage of DCC at asp1290. Stein et al.(2001) concluded that it plays a central role in netrin signaling of axon growth and guidance independent of A2B receptor activation. Protein function: Receptor for netrin required for axon guidance. Mediates axon attraction of neuronal growth cones in the developing nervous system upon ligand binding. Its association with UNC5 proteins may trigger signaling for axon repulsion. It also acts as a dependence receptor required for apoptosis induction when not associated with netrin ligand. Implicated as a tumor suppressor gene. [The UniProt Consortium]