NGF-induced axon growth is mediated by localized inactivation of GSK-3beta and functions of the microtubule plus end binding protein APC. [electronic resource]
Producer: 20040802Description: 897-912 p. digitalISSN:- 0896-6273
- Adenomatous Polyposis Coli -- metabolism
- Analysis of Variance
- Animals
- Antineoplastic Agents -- pharmacology
- Axons -- drug effects
- Blotting, Western -- methods
- Cell Count
- Cells, Cultured
- Cytoskeletal Proteins -- metabolism
- Dose-Response Relationship, Drug
- Drug Interactions
- Embryo, Mammalian
- Enzyme Inhibitors -- pharmacology
- Fluorescent Antibody Technique -- methods
- Ganglia, Spinal -- cytology
- Gene Expression Regulation -- genetics
- Glycogen Synthase Kinase 3 -- metabolism
- Glycogen Synthase Kinase 3 beta
- Green Fluorescent Proteins
- Growth Cones -- drug effects
- Luminescent Proteins -- metabolism
- Mice
- Microtubule-Associated Proteins -- metabolism
- Microtubules -- metabolism
- Models, Neurological
- Mutagenesis, Site-Directed -- physiology
- Nerve Growth Factors -- immunology
- Neurons -- cytology
- Protein Serine-Threonine Kinases -- metabolism
- Proto-Oncogene Proteins -- metabolism
- Proto-Oncogene Proteins c-akt
- Signal Transduction -- genetics
- Trans-Activators -- metabolism
- Transfection -- methods
- Tubulin -- metabolism
- beta Catenin
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Publication Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
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