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RanBPM contributes to TrkB signaling and regulates brain‐derived neurotrophic factor‐induced neuronal morphogenesis and survival
Author(s) -
Yin YuXia,
Sun ZongPeng,
Huang ShuHong,
Zhao Ling,
Geng Zhao,
Chen ZheYu
Publication year - 2010
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2010.06745.x
Subject(s) - tropomyosin receptor kinase b , trk receptor , tropomyosin receptor kinase a , neurotrophin , microbiology and biotechnology , brain derived neurotrophic factor , low affinity nerve growth factor receptor , protein kinase b , neurotrophic factors , biology , tropomyosin receptor kinase c , receptor tyrosine kinase , morphogenesis , nerve growth factor , signal transduction , chemistry , receptor , growth factor , platelet derived growth factor receptor , biochemistry , gene
J. Neurochem. (2010) 114 , 110–121. 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.

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