期刊
JOURNAL OF NEUROSCIENCE
卷 31, 期 29, 页码 10602-10614出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0436-11.2011
关键词
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资金
- National Natural Science Foundation of China [30725020, 31071254, 30900717]
- National 973 Basic Research Program of China [2010CB912004, 2009CB941403]
- National Natural Science Foundation of China for Innovative Research Group [81021001]
- Foundation for Excellent Young Scientist of Shandong Province [BS2010SW022]
- research fund for the Doctoral Program of Higher Education of China [200804221070]
- Independent Innovation Foundation of Shandong University
Brain-derived neurotrophic factor (BDNF), secreted from target tissues, binds and activates TrkB receptors, located on axonal terminals of the innervating neurons, and thereby initiates retrograde signaling. Long-range anterograde transport of TrkB in axons and dendrites requires kinesin-mediated transport. However, it remains unknown whether anterograde TrkB transport mechanisms are the same in axons versus in dendrites. Here, we show that c-Jun NH(2)-terminal kinase-interacting protein 3 (JIP3) binds directly to TrkB, via a minimal 12 aa domain in the TrkB juxtamembrane region, and links TrkB to kinesin-1. The JIP3/TrkB interaction selectively drives TrkB anterograde transport in axons but not in dendrites of rat hippocampal neurons. Moreover, we find that TrkB axonal transport mediated by JIP3 could regulate BDNF-induced Erk activation and axonal filopodia formation. Our findings demonstrate a role for JIP3-mediated TrkB anterograde axonal transport in recruiting more TrkB into distal axons and facilitating BDNF-induced retrograde signaling and synapse modulation, which provides a novel mechanism of how the TrkB anterograde transport can be coupled to BDNF signaling in distal axons.
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