Liver Kinase B1 Functions as a Regulator for Neural Development and a Therapeutic Target for Neural Repair.
Liver Kinase B1 Functions as a Regulator for Neural Development and a Therapeutic Target for Neural Repair.
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肝激酶B1(LKB1)在线虫中又称丝氨酸/苏氨酸激酶11(STK11)和PAR-4，是AMPKs和AMPK相关蛋白的主激酶。LKB1在细胞生长、新陈代谢、极性和肿瘤抑制中起着至关重要的作用。LKB1通过与SAD、NUAK、MARK和其他激酶的下游信号相互作用，在发育过程中调节神经元极化和轴突分支。它还调节雪旺细胞的功能和外周轴突的髓鞘形成。调节LKB1活性已成为修复受损神经系统的一种有吸引力的策略。LKB1上调可增强成年中枢神经系统神经元的再生能力，促进成年中枢神经系统轴突损伤大鼠运动功能的恢复。在这里，我们更新了LKB1调节神经元极化和神经发育的主要细胞和分子机制，以及它对促进成年哺乳动物神经修复、轴突再生和功能恢复的意义。
The liver kinase B1 (LKB1), also known as serine/threonine kinase 11 (STK11) and Par-4 in C. elegans, has been identified as a master kinase of AMPKs and AMPK-related kinases. LKB1 plays a crucial role in cell growth, metabolism, polarity, and tumor suppression. By interacting with the downstream signals of SAD, NUAK, MARK, and other kinases, LKB1 is critical to regulating neuronal polarization and axon branching during development. It also regulates Schwann cell function and the myelination of peripheral axons. Regulating LKB1 activity has become an attractive strategy for repairing an injured nervous system. LKB1 upregulation enhances the regenerative capacity of adult CNS neurons and the recovery of locomotor function in adult rodents with CNS axon injury. Here, we update the major cellular and molecular mechanisms of LKB1 in regulating neuronal polarization and neural development, and the implications thereof for promoting neural repair, axon regeneration, and functional recovery in adult mammals.
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