Author
Listed:
- Amin Fazeli
(Massachusetts Institute of Technology)
- Stephanie L. Dickinson
(Massachusetts Institute of Technology)
- Michelle L. Hermiston
(Washington University School of Medicine)
- Robert V. Tighe
(Massachusetts Institute of Technology)
- Robert G. Steen
(Massachusetts Institute of Technology/Whitehead Institute Genome Center)
- Clayton G. Small
(Massachusetts Institute of Technology)
- Esther T. Stoeckli
(Developmental Biology and Neuroscience, University of California)
- Kazuko Keino-Masu
(Developmental Biology and Neuroscience, University of California
National Defense Medical College)
- Masayuki Masu
(Developmental Biology and Neuroscience, University of California)
- Helen Rayburn
(Massachusetts Institute of Technology)
- Jonathan Simons
(Johns Hopkins University)
- Roderick T. Bronson
(Tufts University Schools of Medicine and Veterinary Medicine)
- Jeffrey I. Gordon
(Washington University School of Medicine)
- Marc Tessier-Lavigne
(Developmental Biology and Neuroscience, University of California)
- Robert A. Weinberg
(Massachusetts Institute of Technology)
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.
Suggested Citation
Amin Fazeli & Stephanie L. Dickinson & Michelle L. Hermiston & Robert V. Tighe & Robert G. Steen & Clayton G. Small & Esther T. Stoeckli & Kazuko Keino-Masu & Masayuki Masu & Helen Rayburn & Jonathan , 1997.
"Phenotype of mice lacking functional Deleted in colorectal cancer (Dec) gene,"
Nature, Nature, vol. 386(6627), pages 796-804, April.
Handle:
RePEc:nat:nature:v:386:y:1997:i:6627:d:10.1038_386796a0
DOI: 10.1038/386796a0
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