1. Phenotype of mice lacking functional Deleted in colorectal cancer (Dcc) gene.
- Author
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Fazeli A, Dickinson SL, Hermiston ML, Tighe RV, Steen RG, Small CG, Stoeckli ET, Keino-Masu K, Masu M, Rayburn H, Simons J, Bronson RT, Gordon JI, Tessier-Lavigne M, and Weinberg RA
- Subjects
- Animals, Axons pathology, Brain abnormalities, Brain embryology, Brain Neoplasms genetics, Cell Adhesion Molecules genetics, Cell Division, Chimera, Chromosome Mapping, Colorectal Neoplasms genetics, DCC Receptor, Gene Targeting, Humans, Intestinal Mucosa pathology, Intestinal Polyps genetics, Mice, Mice, Inbred C57BL, Nerve Growth Factors physiology, Netrin-1, Phenotype, Receptors, Cell Surface metabolism, Spinal Cord abnormalities, Spinal Cord embryology, Cell Adhesion Molecules physiology, Genes, DCC, Intestinal Neoplasms genetics, Mutagenesis, Tumor Suppressor Proteins
- Abstract
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.
- Published
- 1997
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