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NGF-induced axon growth is mediated by localized inactivation of GSK-3beta and functions of the microtubule plus end binding protein APC.

Neuron | Jun 24, 2004

Little is known about how nerve growth factor (NGF) signaling controls the regulated assembly of microtubules that underlies axon growth. Here we demonstrate that a tightly regulated and localized activation of phosphatidylinositol 3-kinase (PI3K) at the growth cone is essential for rapid axon growth induced by NGF. This spatially activated PI3K signaling is conveyed downstream through a localized inactivation of glycogen synthase kinase 3beta (GSK-3beta). These two spatially coupled kinases control axon growth via regulation of a microtubule plus end binding protein, adenomatous polyposis coli (APC). Our results demonstrate that NGF signals are transduced to the axon cytoskeleton via activation of a conserved cell polarity signaling pathway.

Pubmed ID: 15207235 RIS Download

Mesh terms: Adenomatous Polyposis Coli | Analysis of Variance | Animals | Antineoplastic Agents | Axons | Blotting, Western | Cell Count | Cells, Cultured | Cytoskeletal Proteins | Dose-Response Relationship, Drug | Drug Interactions | Embryo, Mammalian | Enzyme Inhibitors | Fluorescent Antibody Technique | Ganglia, Spinal | Gene Expression Regulation | Glycogen Synthase Kinase 3 | Glycogen Synthase Kinase 3 beta | Green Fluorescent Proteins | Growth Cones | Luminescent Proteins | Mice | Microtubule-Associated Proteins | Microtubules | Models, Neurological | Mutagenesis, Site-Directed | Nerve Growth Factors | Neurons | Protein-Serine-Threonine Kinases | Proto-Oncogene Proteins | Proto-Oncogene Proteins c-akt | Signal Transduction | Trans-Activators | Transfection | Tubulin | beta Catenin

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