Signal transduction by L1

Besides adhesive roles in cell cell interaction, L1 functions as a signal transducing receptor providing neurons with cues from their environment for axonal growth and guidance. L1 associates with beta1 integrins on the cell surface to induce a signaling pathway involving sequential activation of pp60csrc, Vav2 -GEF, Rac1, PAK1, MEK and ERK1/2. L1 stimulates cell migration and neurite outgrowth through the MAP kinases ERK1/2. CHL1 also associates with integrins and activates a MAPK signaling pathway via pp60c-src, MEK and ERK1/2. <br>L1 also binds the Sema3A receptor neuropilin1 and acts as an obligate coreceptor to mediate Sema3A induced growth cone collapse and axon repulsion. This repulsion can be converted to attraction by homophilic binding of L1 on an apposing cell in trans with L1 complexed with Neuropilin1 (NP1) in the responding neuron.<br>L1 also interacts with FGF receptor and activates PLC gamma and DAG, resulting in the production of arachidonic acid and subsequent opening of voltage-gated channels.

在细胞间相互作用中，L1除扮演粘附角色外，尚作为信号转导受体，向神经元提供其环境中的线索，以指导轴突的生长与导向。L1与细胞表面的β1整合素结合，诱导一条涉及pp60csrc、Vav2-GEF、Rac1、PAK1、MEK和ERK1/2顺序激活的信号转导途径。L1通过MAP激酶ERK1/2的介导，刺激细胞迁移和神经突的生长。CHL1亦与整合素结合，并通过pp60c-src、MEK和ERK1/2激活MAPK信号转导途径。L1还与Sema3A受体神经突蛋白1结合，充当必需的共受体，介导Sema3A诱导的生长锥塌陷和轴突排斥。这种排斥可通过L1在相对细胞上的同源结合以及与神经突蛋白1（NP1）结合的L1复合物在响应神经元中的异源结合转化为吸引。此外，L1还与FGF受体相互作用，激活PLCγ和DAG，导致花生四烯酸的生成，进而开启电压门控通道。