C-Jun-N-末端激酶 (JNK) 是丝裂原激活蛋白激酶家族的成员，与神经系统和神经退行性病理学以及癌症进展显着相关。然而，JNK 在生理条件下发挥着关键作用，特别是在中枢神经系统 (CNS) 中，它们在胚胎发生和成体阶段控制神经增殖和分化方面至关重要。这些过程控制中枢神经系统的发育，避免神经发育障碍。 JNK 是维持成人神经干细胞 (NSC) 和神经祖细胞 (NPC) 正常活性的关键，从而保持大脑的可塑性和稳态。本综述强调了 JNK 与上游和下游分子的相互作用如何作为一种调节机制来管理中枢神经系统发育期间和成人神经源性生态位中 NSC/NPC 的自我更新能力和分化。有证据表明，JNK 依赖于非经典 Wnt 成分、Fbw7 泛素连接酶和 WDR62 支架蛋白，调节转录因子和细胞骨架蛋白等底物。因此，了解哪些途径和分子与 JNK 相互作用将带来有关 JNK 激活如何协调中枢神经系统发育和大脑疾病中发生的神经元过程的知识。版权所有 © 2024。由 Elsevier Inc. 出版。

C-Jun-N-terminal-kinases (JNKs), members of the mitogen-activated-protein-kinase family, are significantly linked with neurological and neurodegenerative pathologies and cancer progression. However, JNKs serve key roles under physiological conditions, particularly within the central-nervous-system (CNS), where they are critical in governing neural proliferation and differentiation during both embryogenesis and adult stages. These processes control the development of CNS, avoiding neurodevelopment disorders. JNK are key to maintain the proper activity of neural-stem-cells (NSC) and neural-progenitors (NPC) that exist in adults, which keep the convenient brain plasticity and homeostasis. This review underscores how the interaction of JNK with upstream and downstream molecules acts as a regulatory mechanism to manage the self-renewal capacity and differentiation of NSC/NPC during CNS development and in adult neurogenic niches. Evidence suggests that JNK is reliant on non-canonical Wnt components, Fbw7-ubiquitin-ligase, and WDR62-scaffold-protein, regulating substrates such as transcription factors and cytoskeletal proteins. Therefore, understanding which pathways and molecules interact with JNK will bring knowledge on how JNK activation orchestrates neuronal processes that occur in CNS development and brain disorders.Copyright © 2024. Published by Elsevier Inc.