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Role of Unc51.1 and its binding partners in CNS axon outgrowth.

Genes & development | Mar 1, 2004

Previous studies showed that the serine/threonine kinase Unc51.1 is one of the earliest genes in neuronal differentiation and is required for granule cell axon formation. To examine the mechanism of Unc51.1 regulation of axon extension, we have identified two direct binding partners. The first, SynGAP, a negative regulator of Ras, is expressed within axons and growth cones of developing granule cells. Overexpression of SynGAP blocks neurite outgrowth by a mechanism that involves Ras-like GTPase cascade. The second binding partner is a PDZ domain-containing scaffolding protein, Syntenin, that binds Rab5 GTPase, the activity of which is attenuated by SynGAP. Thus, our results demonstrate that the Unc51.1-containing protein complex governs axon formation via Ras-like GTPase signaling and through regulation of the Rab5-mediated endocytic pathways within developing axons.

Pubmed ID: 15014045 RIS Download

Mesh terms: Animals | Autophagy-Related Protein-1 Homolog | Axons | Carrier Proteins | Cell Differentiation | Central Nervous System | Embryonic and Fetal Development | Endocytosis | GTPase-Activating Proteins | Mice | Nerve Tissue Proteins | Neurons | Protein Binding | Protein-Serine-Threonine Kinases | Receptors, Cell Surface | Syntenins | rab5 GTP-Binding Proteins | ras GTPase-Activating Proteins | ras Proteins

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Associated grants

  • Agency: NINDS NIH HHS, Id: R01 NS039991
  • Agency: NINDS NIH HHS, Id: NS39991

Gene Ontology (Data, Gene Annotation)

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