The dual leucine zipper-bearing kinase (DLK) and leucine zipper-bearing kinase (LZK) are evolutionarily conserved MAPKKKs of the mixed-lineage kinase family. Acting upstream of stress-responsive JNK and p38 MAP kinases, DLK and LZK have emerged as central players in neuronal responses to a variety of acute and traumatic injuries. Recent studies also implicate their function in astrocytes, microglia, and other nonneuronal cells, reflecting their expanding roles in the multicellular response to injury and in disease. Of particular note is the potential link of these kinases to neurodegenerative diseases and cancer. It is thus critical to understand the physiological contexts under which these kinases are activated, as well as the signal transduction mechanisms that mediate specific functional outcomes. In this review we first provide a historical overview of the biochemical and functional dissection of these kinases. We then discuss recent findings on regulating their activity to enhance cellular protection following injury and in disease, focusing on but not limited to the nervous system.

中文翻译：

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多任务处理：神经元发育和压力管理中的双亮氨酸拉链激酶。

双亮氨酸拉链激酶（DLK）和亮氨酸拉链激酶（LZK）是混合谱系激酶家族的进化保守MAPKKKs。DLK和LZK在应激反应性JNK和p38 MAP激酶的上游起作用，已成为对各种急性和创伤性损伤的神经元反应的主要参与者。最近的研究还暗示它们在星形胶质细胞，小胶质细胞和其他非神经元细胞中的功能，反映了它们在对损伤和疾病的多细胞反应中的扩展作用。特别值得注意的是这些激酶与神经退行性疾病和癌症的潜在联系。因此，了解这些激酶被激活的生理环境以及介导特定功能结果的信号转导机制至关重要。在这篇综述中，我们首先提供这些激酶的生化和功能解剖的历史概述。然后，我们讨论了有关调节其活性以增强损伤后和疾病中的细胞保护作用的最新发现，重点是但不限于神经系统。