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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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|
|Date:||24 April 1997|
|Deposited On:||11 Feb 2008 12:14|
|Last Modified:||28 Nov 2013 00:56|
|Publisher:||Nature Publishing Group|
|Citations:||Web of Science®. Times Cited: 487|
Scopus®. Citation Count: 496
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