Literature DB >> 9126737

Phenotype of mice lacking functional Deleted in colorectal cancer (Dcc) gene.

A Fazeli1, S L Dickinson, M L Hermiston, R V Tighe, R G Steen, C G Small, E T Stoeckli, K Keino-Masu, M Masu, H Rayburn, J Simons, R T Bronson, J I Gordon, M Tessier-Lavigne, R A Weinberg.   

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.

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Year:  1997        PMID: 9126737     DOI: 10.1038/386796a0

Source DB:  PubMed          Journal:  Nature        ISSN: 0028-0836            Impact factor:   49.962


  232 in total

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9.  MARCKS Is Necessary for Netrin-DCC Signaling and Corpus Callosum Formation.

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10.  The Cables gene on chromosome 18q is silenced by promoter hypermethylation and allelic loss in human colorectal cancer.

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