RanBPM contributes to TrkB signaling and regulates brain-derived neurotrophic factor-induced neuronal morphogenesis and survival.

Tropomyosin-related kinase (Trk) B is a receptor tyrosine kinase for brain-derived neurotrophic factor (BDNF) which plays a critical role in neuronal survival, differentiation and morphogenesis. Ran-binding protein in the microtubule-organizing center (RanBPM) is a cytosolic scaffold protein that has been shown to interact with protein-tyrosine kinase receptor MET, Axl/Sky, and ...
TrkA in addition to the pan-neurotrophin receptor pan-neurotrophin receptor 75 kDa. In this study, we report RanBPM is a novel TrkB-interacting protein that contributes to BDNF-induced MAPK and Akt activation together with neuronal morphogenesis and survival. Over-expression of RanBPM in PC1210 cells (PC12 cells stably over-expressing TrkB) can significantly enhance BDNF-induced MAPK and Akt activation. Moreover, RanBPM can promote BDNF-induced hippocampal neuronal morphogenesis and enhance BDNF-mediated trophic effects after serum deprivation, while siRNA knock down of RanBPM in cells has the opposite effects. Together, these results suggest that RanBPM may modulate TrkB-mediated downstream signaling and biological functions.
Mesh Terms:
Adaptor Proteins, Signal Transducing, Animals, Brain-Derived Neurotrophic Factor, Cell Differentiation, Cell Survival, Cells, Cultured, Cytoskeletal Proteins, Dendrites, Enzyme Activation, Hippocampus, Humans, Mitogen-Activated Protein Kinases, Neurons, Nuclear Proteins, Phosphatidylinositol 3-Kinases, Protein Interaction Mapping, Proto-Oncogene Proteins c-akt, Rats, Receptor, trkB, Signal Transduction
J. Neurochem.
Date: Jul. 01, 2010
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