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Role of L1CAM for axon sprouting and branching

机译：L1CAM在轴突发芽和分支中的作用

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The central nervous system (CNS) has been traditionally considered as an organ that fails to regenerate in response to injury. Indeed, the lesioned CNS faces a number of obstacles during regeneration, including an overall non-permissive environment for axonal regeneration. However, research during the last few decades has identified axon sprouting as an anatomical correlate for the regenerative capability of the CNS to establish new connections. The immunoglobulin superfamily member L1CAM has been shown to promote the capability of neurons for regenerative axon sprouting and to improve behavioral outcomes after CNS injury. Here, we discuss the cell-autonomous role of L1CAM for axon sprouting in experimental rodent injury models and highlight the molecular interactions of L1CAM with ankyrins, ezrin-radixin-moesin proteins and the Sema3A/Neuropilin ligand-receptor complex in the context of axonal branching.
机译：传统上，中枢神经系统（CNS）被视为无法响应受伤而再生的器官。实际上，病变的中枢神经系统在再生期间面临许多障碍，包括轴突再生的整个非许可环境。然而，在过去的几十年中的研究已将轴突发芽与中枢神经系统建立新连接的再生能力在解剖上相关。免疫球蛋白超家族成员L1CAM已显示出促进神经元再生轴突发芽的能力，并改善中枢神经系统损伤后的行为结局。在这里，我们讨论L1CAM在实验性啮齿动物损伤模型中对轴突萌发的细胞自主作用，并强调在轴突分支的情况下，L1CAM与锚蛋白，ezrin-radixin-moesin蛋白和Sema3A / Neuropilin配体-受体复合物的分子相互作用。 。

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