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.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Animals
-
Axons / pathology
-
Brain / abnormalities
-
Brain / embryology
-
Brain Neoplasms / genetics
-
Cell Adhesion Molecules / genetics
-
Cell Adhesion Molecules / physiology*
-
Cell Division
-
Chimera
-
Chromosome Mapping
-
Colorectal Neoplasms / genetics
-
DCC Receptor
-
Gene Targeting
-
Genes, DCC*
-
Humans
-
Intestinal Mucosa / pathology
-
Intestinal Neoplasms / genetics*
-
Intestinal Polyps / genetics
-
Mice
-
Mice, Inbred C57BL
-
Mutagenesis*
-
Nerve Growth Factors / physiology
-
Netrin-1
-
Phenotype
-
Receptors, Cell Surface / metabolism
-
Spinal Cord / abnormalities
-
Spinal Cord / embryology
-
Tumor Suppressor Proteins*
Substances
-
Cell Adhesion Molecules
-
DCC Receptor
-
DCC protein, human
-
Dcc protein, mouse
-
NTN1 protein, human
-
Nerve Growth Factors
-
Ntn1 protein, mouse
-
Receptors, Cell Surface
-
Tumor Suppressor Proteins
-
Netrin-1