A dual leucine kinase-dependent axon self-destruction program promotes Wallerian degeneration.

A dual leucine kinase-dependent axon self-destruction program promotes Wallerian degeneration.
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DOI:
10.1038/nn.2290
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发表时间:
2009-04
影响因子:
25
通讯作者:
DiAntonio, Aaron
DiAntonio, Aaron
中科院分区:
医学1区
文献类型:
--
作者:
Miller, Bradley R.;Press, Craig;Daniels, Richard W.;Sasaki, Yo;Milbrandt, Jeffrey;DiAntonio, Aaron

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轴突变性是许多常见神经疾病的基础,但协调轴突变性的信号通路尚不清楚。我们证明了双重亮氨酸激酶(DLK)促进了果蝇和小鼠切断的轴突的退化,其靶标JNK促进了轴突的局部退化,因为它们承诺退化。该途径还促进化疗后的变性,因此可能是一般轴突自毁计划的一个组成部分。
Axon degeneration underlies many common neurological disorders, but the signaling pathways that orchestrate axon degeneration are unknown. We demonstrate that the dual leucine kinase (DLK) promotes degeneration of severed axons in Drosophila and mice, and its target JNK promotes degeneration locally in axons as they commit to degenerate. This pathway also promotes degeneration after chemotherapy exposure, and thus may be a component of a general axon self-destruction program.
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