Human synapsin I mediates the function of nuclear respiratory factor 1 in neurite outgrowth in neuroblastoma IMR-32 cells

Jen Ling Wang, Wen Teng Chang, Chih Wei Tong, Kimitoshi Kohno, A-Min Huang

研究成果: Article同行評審

10 引文 斯高帕斯(Scopus)

摘要

Nuclear respiratory factor (NRF)-1 is a transcription factor with a novel function in neurite outgrowth. Synapsin I protein is a well-known phosphoprotein in neuronal terminals and has been implicated in neuronal differentiation. Human synapsin I gene promoter has a putative NRF-1 responsive element (NRE), but it is not known whether this NRE is functional. We hypothesized that synapsin I is downstream of NRF-1 and mediates its function in neurite outgrowth. Gel electrophoretic mobility shift assays, chromatin immunoprecipitation, site-directed mutagenesis, and promoter studies indicated that NRF-1 is a positive regulator of synapsin I promoter. Exogenous NRF-1 overexpression increased synapsin I protein levels in IMR-32 and HEK293T cells. Serum deprivation, which induces neurite outgrowth in IMR-32 cells, increased the binding activity of NRF-1 to synapsin I NRE and induced alternating synapsin I protein expression. Down-regulating synapsin I expression markedly decreased the percentage of neurite-bearing cells and the length of the longest neurite in IMR-32 cells that stably or transiently overexpressed NRF-1. We conclude that the human synapsin I gene is positively regulated by NRF-1 and mediates the function of NRF-1 in neurite outgrowth.

原文English
頁(從 - 到)2255-2263
頁數9
期刊Journal of Neuroscience Research
87
發行號10
DOIs
出版狀態Published - 2009 八月 1

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience

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