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首页> 外文期刊>Neuron >Dual Leucine Zipper Kinase Is Required for Retrograde Injury Signaling and Axonal Regeneration
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Dual Leucine Zipper Kinase Is Required for Retrograde Injury Signaling and Axonal Regeneration

机译：逆转录损伤信号转导和轴突再生需要双亮氨酸拉链激酶。

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Here we demonstrate that the dual leucine zipper kinase (DLK) promotes robust regeneration of peripheral axons after nerve injury in mice. Peripheral axon regeneration is accelerated by prior injury; however, DLK KO neurons do not respond to a preconditioning lesion with enhanced regeneration in vivo or in vitro. Assays for activation of transcription factors in injury-induced proregenerative pathways reveal that loss of DLK abolishes upregulation of p-STAT3 and p-cJun in the cell body after axonal injury. DLK is not required for the phosphorylation of STAT3 at the site of nerve injury but is necessary for retrograde transport of p-STAT3 to the cell body. These data demonstrate that DLK enhances regeneration by promoting a retrograde injury signal that is required for the activation of the neuronal proregenerative program. Peripheral nerve injury activates a neuronal transcriptional program that enhances axonal regeneration. Shin et al. report that dual leucine zipper kinase promotes axon regeneration by regulating retrograde transport of injury signals in mammals.
机译：在这里，我们证明了双亮氨酸拉链激酶（DLK）促进小鼠神经损伤后外周轴突的强健再生。先前的损伤会促进周围轴突的再生;然而，DLK KO神经元对体内或体外再生能力增强的预适应病变无反应。损伤诱导的再生途径中转录因子激活的测定表明，DLK的丧失消除了轴突损伤后细胞体内p-STAT3和p-cJun的上调。 DLK对于神经损伤部位的STAT3磷酸化不是必需的，但对于p-STAT3逆向运输至细胞体则是必需的。这些数据表明，DLK通过促进神经元再生程序激活所需的逆行损伤信号来增强再生。周围神经损伤会激活神经元转录程序，从而增强轴突再生。 Shin等。报告指出，双亮氨酸拉链激酶通过调节哺乳动物损伤信号的逆行转运来促进轴突再生。

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