Taiji M, Taiji K, Deyerle K L, Bothwell M
Department of Physiology and Biophysics, School of Medicine, University of Washington, Seattle 98195.
Mol Cell Biol. 1992 May;12(5):2193-202. doi: 10.1128/mcb.12.5.2193-2202.1992.
The human neuroblastoma cell line CHP100 provides a useful model system in which to study the molecular mechanisms of transcriptional regulation of the low-affinity nerve growth factor receptor (NGFR) gene during neuronal development. Basic fibroblast growth factor (bFGF) induced morphological changes in CHP100 cells, including flattening of cell bodies and neurite outgrowth. bFGF also increased p75NGFR immunoreactivity, as assessed by immunocytochemistry, and increased p75NGFR mRNA levels, as assessed by Northern (RNA) blot analysis. A chimeric gene consisting of 6.7 kb of the 5'-flanking region of the human NGFR gene linked to the chloramphenicol acetyltransferase gene was constructed. In stable transformants of CHP100 cells, 10 ng of bFGF per ml induced an eightfold increase in chloramphenicol acetyltransferase activity. These results indicate that upstream elements of the NGFR gene mediate transcriptional regulation by bFGF.
人神经母细胞瘤细胞系CHP100提供了一个有用的模型系统,用于研究神经元发育过程中低亲和力神经生长因子受体(NGFR)基因转录调控的分子机制。碱性成纤维细胞生长因子(bFGF)诱导CHP100细胞发生形态学变化,包括细胞体变平及神经突生长。通过免疫细胞化学评估,bFGF还增加了p75NGFR免疫反应性,通过Northern(RNA)印迹分析评估,bFGF增加了p75NGFR mRNA水平。构建了一个由6.7 kb人NGFR基因5'侧翼区域与氯霉素乙酰转移酶基因相连的嵌合基因。在CHP100细胞的稳定转化体中,每毫升10 ng的bFGF诱导氯霉素乙酰转移酶活性增加了八倍。这些结果表明,NGFR基因的上游元件介导bFGF的转录调控。