A sequence-specific splicing activator, Tra2β, is up-regulated in response to nerve injury
A sequence-specific splicing activator, Tra2β, is up-regulated in response to nerve injury
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DOI：
10.1016/s0169-328x(98)00255-1
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发表时间：
1998-11-20
期刊：
影响因子：
--
通讯作者：
Kiyama, H
中科院分区：
文献类型：
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作者：
Kiryu-Seo, S;Matsuo, N;Kiyama, H
Tra2 beta 是第一个被证明能够以序列特异性方式激活 mRNA 剪接的哺乳动物蛋白。舌下神经损伤后，受损运动神经元中 Tra2 β mRNA 的表达短暂升高。术后第3天至21天观察到Tra2βmRNA的表达上调。除了PNS中的神经损伤外，CNS中的脑损伤也增强了Tra2βmRNA的表达。本研究可能是第一个观察结果，表明序列特异性剪接激活剂的表达在神经元细胞中响应神经损伤而增强，并表明 Tra2 β 可能参与损伤特异性剪接模式的控制，以表达再生所需的分子。 (C) 1998 Elsevier Science B.V. 保留所有权利。
Tra2 beta is the first mammalian protein which is proved to activate mRNA splicing in sequence-specific manner. Following hypoglossal nerve injury, the expression of Tra2 beta mRNA was elevated in injured motoneurons transiently. The up-regulation of Tra2 beta mRNA was observed from post-operative day 3 to 21. In addition to the nerve injury in PNS, a brain lesion in CNS also enhanced the expression of Tra2 beta mRNA. The present study could be the first observation showing that an expression of the sequence-specific splicing activator is enhanced in neuronal cells in response to nerve injury, and indicates that Tra2 beta may participate in the control of injury-specific splicing patterns in order to express molecules which are necessary for regeneration. (C) 1998 Elsevier Science B.V. All rights reserved.