Kiryu-Seo S, Matsuo N, Wanaka A, Ogawa S, Tohyama M, Kiyama H
Department of Anatomy, Asahikawa Medical college, Nishikagura 4-5-3-11, Asahikawa, 078-8510, Japan.
Brain Res Mol Brain Res. 1998 Nov 20;62(2):220-3. doi: 10.1016/s0169-328x(98)00255-1.
Tra2beta is the first mammalian protein which is proved to activate mRNA splicing in sequence-specific manner. Following hypoglossal nerve injury, the expression of Tra2beta mRNA was elevated in injured motoneurons transiently. The up-regulation of Tra2beta 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 Tra2beta 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 Tra2beta may participate in the control of injury-specific splicing patterns in order to express molecules which are necessary for regeneration.
Tra2β是首个被证实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，Tra2β mRNA在损伤的运动神经元中短暂升高。术后第3天至21天观察到Tra2β mRNA上调。除了周围神经系统的神经损伤外，中枢神经系统的脑损伤也增强了Tra2β mRNA的表达。本研究可能是首次观察到序列特异性剪接激活剂在神经元细胞中响应神经损伤而表达增强，并表明Tra2β可能参与损伤特异性剪接模式的调控，以表达再生所需的分子。
