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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Chen, Bing Zhao, Ling Li, Xian Ji, Yun-song Li, Na Xu, Xu-feng Chen, Zhe-yu |
| Description | Author Affiliation: Chen B ( From the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China.); Zhao L ( From the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China.); Li X ( From the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China.); Ji YS ( From the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China.); Li N ( From the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China.); Xu XF ( From the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China.); Chen ZY ( From the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China zheyuchen@sdu.edu.cn.) |
| Abstract | Nerve growth factor (NGF) promotes the survival, maintenance, and neurite outgrowth of sensory and sympathetic neurons, and the effects are mediated by TrkA receptor signaling. Thus, the cell surface location of the TrkA receptor is crucial for NGF-mediated functions. However, the regulatory mechanism underlying TrkA cell surface levels remains incompletely understood. In this study, we identified syntaxin 8 (STX8), a Q-SNARE protein, as a novel TrkA-binding protein. Overexpression and knockdown studies showed that STX8 facilitates TrkA transport from the Golgi to the plasma membrane and regulates the surface levels of TrkA but not TrkB receptors. Furthermore, STX8 modulates downstream NGF-induced TrkA signaling and, consequently, the survival of NGF-dependent dorsal root ganglia neurons. Finally, knockdown of STX8 in rat dorsal root ganglia by recombinant adeno-associated virus serotype 6-mediated RNA interference led to analgesic effects on formalin-induced inflammatory pain. These findings demonstrate that STX8 is a modulator of TrkA cell surface levels and biological functions. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 28 |
| Volume Number | 289 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2014-07-11 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Ganglia, Spinal Metabolism Neurons Pain Qa-SNARE Proteins Receptor, TrkA Signal Transduction Animals Fixatives Adverse Effects Pharmacology Formaldehyde Pathology Gene Knockdown Techniques HEK293 Cells Inflammation Chemically Induced Genetics PC12 Cells Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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