| First Author | Fazeli A | Year | 1997 |
| Journal | Nature | Volume | 386 |
| Issue | 6627 | Pages | 796-804 |
| PubMed ID | 9126737 | Mgi Jnum | J:39765 |
| Mgi Id | MGI:87114 | Doi | 10.1038/386796a0 |
| Citation | Fazeli A, et al. (1997) Phenotype of mice lacking functional Deleted in colorectal cancer (Dcc) gene. Nature 386(6627):796-804 |
| abstractText | The DCC (Deleted in colorectal cancer) gene was first identified as a candidate for a tumour-suppressor gene on human chromosome 18q. More recently, in vitro studies In rodents have provided evidence that DCC might function as a receptor for the axonal chemoattractant netrin-1. Inactivation of the murine Dcc gene caused defects in axonal projections that are similar to those observed in netrin-1-deficient mice but did not affect growth, differentiation, morphogenesis or tumorigenesis in mouse intestine. These observations fail to support a tumour- suppressor function for Dcc, but are consistent with the hypothesis that DCC Is a component of a receptor for netrin-1. |
