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首页> 外文期刊>European Journal of Cell Biology: Journal of Deutsche Gesellschaft fur Elektronenmikroskopie: Journal of Deutsche Gesellschaft fur Zellbiologie >Intact Ras function is required for sustained activation and nucleartranslocation of extracellular signal-regulated kinases in nerve growthfactor-stimulated PC12 cells
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Intact Ras function is required for sustained activation and nucleartranslocation of extracellular signal-regulated kinases in nerve growthfactor-stimulated PC12 cells

机译：完整的Ras功能对于神经生长因子刺激的PC12细胞中胞外信号调节激酶的持续激活和核转运是必需的

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摘要

PC12 pheochromocytoma cell lines expressing the dominant negative Ha-Ras Asn-17 protein at different levels were used in this study to analyze the relationship between nerve growth factor (NGF)-induced activation of members of the mitogen-activated protein kinase (MAPK) family, and neuritogenesis, In wild-type PC12 cells. NGF rapidly stimulated the extracellular signal-regulated kinases (ERKs), Kinase activation was sustained and was followed by the translocation of ERK 1 and ERK 2 into the nucleus ultimately leading to neurite outgrowth. In cells expressing relatively high levels of the inhibitory Res protein, NGF stimulation of ERK 1 and ERK 2 as well as nuclear translocation of these protein kinases were greatly inhibited, In contrast, in PC12 subclones expressing low amounts of Ha-Ras Asn-17 the peak of ERK activation was only slightly reduced, but became transient in nature and was not followed by nuclear translocation of ERKs 1 and 2. Since all PC12 subclones expressing detectable levels of the dominant inhibitory Ras protein are resistant to NGF induction of neurite formation, our observations support the notion that sustained activation and translocation of ERKs into the nucleus are essential for NGF-induced neuronal differentiation of PC12 cells.
机译：使用PC12嗜铬细胞瘤细胞系以不同水平表达占主导地位的阴性Ha-Ras Asn-17蛋白，来分析神经生长因子（NGF）诱导的丝裂原活化蛋白激酶（MAPK）家族成员之间的关系。和神经发生，在野生型PC12细胞中。 NGF迅速刺激细胞外信号调节激酶（ERKs），激酶激活得以持续，随后ERK 1和ERK 2易位进入细胞核，最终导致神经突生长。在表达相对高水平的抑制性Res蛋白的细胞中，NGF对ERK 1和ERK 2的刺激以及这些蛋白激酶的核易位被大大抑制。相反，在表达少量Ha-Ras Asn-17的PC12亚克隆中ERK激活的峰值仅略有降低，但在性质上却是短暂的，并没有随后发生ERK 1和2的核易位。由于所有表达可检测水平的主要抑制性Ras蛋白的PC12亚克隆均抗NGF诱导的神经突形成。观察结果支持以下观念：ERK的持续激活和易位到核中对于NGF诱导PC12细胞的神经元分化至关重要。

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