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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.

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

Authors

  • Zhou FQ
  • Zhou J
  • Dedhar S
  • Wu YH
  • Snider WD

Journal

Neuron

Publication Data

June 24, 2004

Associated Grants

  • Agency: NINDS NIH HHS, Id: NS031768
  • Agency: NINDS NIH HHS, Id: P30 NS045892

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
  • 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