RanBPM contributes to TrkB signaling and regulates brain-derived neurotrophic factor-induced neuronal morphogenesis and survival.
J Neurochem
; 114(1): 110-21, 2010 Jul.
Article
en En
| MEDLINE
| ID: mdl-20403074
ABSTRACT
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.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proteínas Nucleares
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Factor Neurotrófico Derivado del Encéfalo
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Receptor trkB
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Proteínas del Citoesqueleto
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Proteínas Adaptadoras Transductoras de Señales
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Neuronas
Límite:
Animals
/
Humans
Idioma:
En
Revista:
J Neurochem
Año:
2010
Tipo del documento:
Article
País de afiliación:
China