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Fazeli, A; Dickinson, S L; Hermiston, M L; Tighe, R V; Steen, R G; Small, C G; Stoeckli, E T; Keino-Masu, K; Masu, M; Rayburn, H; Simons, J; Bronson, R T; Gordon, J I; Tessier-Lavigne, M; Weinberg, R A (1997). Phenotype of mice lacking functional Deleted in colorectal cancer (Dcc) gene. Nature, 386(6627):796-804.

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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.

Item Type:Journal Article, refereed, original work
Communities & Collections:07 Faculty of Science > Institute of Molecular Life Sciences
DDC:570 Life sciences; biology
Language:English
Date:24 April 1997
Deposited On:11 Feb 2008 12:14
Last Modified:28 Nov 2013 00:56
Publisher:Nature Publishing Group
ISSN:0028-0836
Publisher DOI:10.1038/386796a0
PubMed ID:9126737
Citations:Web of Science®. Times Cited: 491
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Scopus®. Citation Count: 500

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