Focal adhesion kinase in netrin-1 signaling
Copyright policy )Focal adhesion kinase in netrin-1 signaling
Netrins are a family of secreted molecules that are important for axonal outgrowth and guidance in the developing nervous system. However, the signaling mechanisms that lie immediately downstream of netrin receptors remain poorly understood. Here we report that the netrin receptor DCC (deleted in colorectal cancer) interacts with the focal adhesion kinase (FAK), a kinase implicated in regulating cell adhesion and migration. FAK was expressed in developing brains and was localized with DCC in cultured neurons. Netrin-1 induced FAK and DCC tyrosine phosphorylation. Disruption of FAK signaling abolished netrin-1-induced neurite outgrowth and attractive growth cone turning. Taken together, these results indicate a new signaling mechanism for DCC, in which FAK is activated upon netrin-1 stimulation and mediates netrin-1 function; they also identify a critical role for FAK in axon navigation.
- Alabama Agricultural and Mechanical University United States
- Georgia Regents University United States
- University of Alabama at Birmingham United States
- University of Mary United States
- Washington University in St. Louis United States
Cerebral Cortex, Dose-Response Relationship, Drug, Blotting, Western, Green Fluorescent Proteins, Cell Count, Chick Embryo, Embryo, Mammalian, Axons, Coculture Techniques, Enzyme Activation, Gene Expression Regulation, Culture Media, Conditioned, Focal Adhesion Kinase 1, Focal Adhesion Protein-Tyrosine Kinases, Animals, Humans, Drug Interactions, Female, Enzyme Inhibitors, Cells, Cultured
Cerebral Cortex, Dose-Response Relationship, Drug, Blotting, Western, Green Fluorescent Proteins, Cell Count, Chick Embryo, Embryo, Mammalian, Axons, Coculture Techniques, Enzyme Activation, Gene Expression Regulation, Culture Media, Conditioned, Focal Adhesion Kinase 1, Focal Adhesion Protein-Tyrosine Kinases, Animals, Humans, Drug Interactions, Female, Enzyme Inhibitors, Cells, Cultured
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