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关注:1 2013-05-23 12:21

求翻译:Both neurotrophic factors and activity regulate synaptogenesis. At neuromuscular synapses, the neural factor agrin released from motor neuron terminals stimulates postsynaptic specialization by way of the muscle specific kinase MuSK. In addition, activity through acetylcholine receptors (AChRs) has been implicated in the stabilization of pre- and postsynaptic contacts on muscle at various stages of development. We show here that activation of AChRs with specific concentrations of nicotine is sufficient to induce AChR aggregation and that this induction requires the function of L-type calcium channels (L-CaChs). Furthermore, AChR function is required for agrin induced AChR aggregation in C2 muscle cells. The same concentrations of nicotine did not induce observable tyrosine phosphorylation on either MuSK or the AChR beta subunit, suggesting significant differences between the mechanisms of agrin and activity induced aggregation. The AChR/L-CaCh pathway provides a mechanism by which neuromuscular signal transmission can act in concert with the agrin-MuSK signaling cascade to regulate NMJ formation是什么意思?

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Both neurotrophic factors and activity regulate synaptogenesis. At neuromuscular synapses, the neural factor agrin released from motor neuron terminals stimulates postsynaptic specialization by way of the muscle specific kinase MuSK. In addition, activity through acetylcholine receptors (AChRs) has been implicated in the stabilization of pre- and postsynaptic contacts on muscle at various stages of development. We show here that activation of AChRs with specific concentrations of nicotine is sufficient to induce AChR aggregation and that this induction requires the function of L-type calcium channels (L-CaChs). Furthermore, AChR function is required for agrin induced AChR aggregation in C2 muscle cells. The same concentrations of nicotine did not induce observable tyrosine phosphorylation on either MuSK or the AChR beta subunit, suggesting significant differences between the mechanisms of agrin and activity induced aggregation. The AChR/L-CaCh pathway provides a mechanism by which neuromuscular signal transmission can act in concert with the agrin-MuSK signaling cascade to regulate NMJ formation
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  • 匿名
2013-05-23 12:26:38
神经营养因子及活性调节突触。在神经肌肉突触释放运动神经元码头的神经因子集聚蛋白刺激肌肉特定激酶麝香的方式的突触后专业化。此外,通过乙酰胆碱受体 (AChRs) 的活动已经涉及到在前和突触后联系上肌肉处于不同的发展阶段的稳定。我们在这里显示 AChRs 与特定浓度烟碱激活是足以诱发美洲人权聚合,此感应需要 L-型钙通道 (L CaChs) 的功能。此外,需要为 C2 肌肉细胞集聚蛋白诱导美洲人权聚合美洲人权功能。尼古丁的相同浓度并不吸引可观察到的酪氨酸磷酸化在麝香或美洲人权 beta 亚基,暗示机制集聚蛋白和活动之间的重大差异致聚合。美洲人权/L-捞途径提供一种机制的神经肌肉的信号传输可以按照音乐会与集聚蛋白麝香以规管 NMJ 形成的信号级联
 
 
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