The DCC gene is composed of 29 exons spanning in a region of 1.2 million bp. The promoter contains a CpG island located -72 bp to +217 bp relative to the transcription startsite.

The complete transcribed mRNA is 5693 bp long.

Splice variants:
13 splice variants have been documented.

DCC encodes a 158.5 kDa Type I membrane protein of 1447 amino acids with an extracellular (1100 amino acids), transmembrane and cytoplasmic (325 amino acids) domain. The extracellular domain includes four immunoglobulin-like domains and six fibronectin type III-like motifs. The cytoplasmic domain is composed of three conserved domains named P1, P2 and P3.

Expression is detected in many tissues (testis, lung, colon, esophagus, skeletal muscle) but is highest in normal brain tissue. Most tissues express low levels of transcripts and proteins.

Cell surface.

DCC is a member of the immunoglobulin superfamily of cell adhesion molecules and acts as a transmembrane dependence receptor for netrins, key factors in the regulation of axon guidance during development of the central nerve system.
In response to netrin-1, DCC becomes tyrosine phosphorylated, localizes to lipid rafts and selectively interacts with the Src family kinases Fyn and Lck to mediate axon attraction.
Furthermore DCC induces apoptosis when unbound to its ligand netrin-1. The DCC cytoplasmic domain is required for the induction of apoptosis and contains a caspase cleavage site which is recognized by caspase 3 in vitro. Upstream of the caspase cleavage domain a proapoptotic domain named addiction dependence domain (ADD) is located, which interacts with caspase 9 in the absence of Netrin-1 and binds DCC-interacting protein-13a (DIP13-a) to mediate DCC-induced cell death.
DCCs downstream effects involve MAPK activation and subsequent activation of the transcription factor Elk-1 and SRE regulated gene expression.

DCC has a homolog in mammals named neogin and is conserved in chimpanzee, dog, cow, mouse, rat, zebrafish, Caenorhabditis elegans (UNC40) and Drosophila (Frazzled).

DCC mutations rarely occur in cancer. In colorectal cancer (CRC) the most common somatic mutations are 120 to 300 bp expansions in a dinucleotide repeat tract located in an intron region immediately downstream of exon 7. Expansions are present in 10-15 % of CRCs which are cancers with microsatellite instability.