通过逆行激活体质亲子亡信号的轴突退化
David J Simon1, Jason Pitts1, Nicholas T Hertz1
1Laboratory of Brain Development and Repair, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Cell
|February 23, 2016
概括
细胞体,不仅仅是轴突, 积极控制轴突退化. 神经营养支持的丧失会触发细胞体的逆向信号,从而启动轴突的移除.
科学领域:
- 神经科学
- 细胞生物学
- 发育生物学
背景情况:
- 感官轴突的发展涉及对神经营养因素的竞争.
- 局部神经质蛋白缺失通常会引发酶依赖的轴突退化.
- 现有的模型表明轴突退化的信号存在于轴突本身.
研究的目的:
- 为了研究细胞体在神经质剥夺时调节轴突退化的作用.
- 为了阐明轴突退化的信号通路.
主要方法:
- 研究了感官轴突退化的信号通路.
- 专注于细胞体和亡机制的作用.
主要成果:
- 在局部剥夺时的轴突退化受到细胞体的积极控制.
- 对细胞体进行逆行信号.
- 细胞体上升调节子,而子只限于细胞体.
- Puma 克服了 Bcl-xL 和 Bcl-w 的抑制,从而启动了前级的亲退行信号.
结论:
- 细胞体是轴突退化的关键门卫.
- 来自被剥夺的轴突的逆行信号激活了体质亡途径.
- 细胞体通过像Puma这样的前级因子调节轴突的移除.
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