Activation of the repulsive receptor Roundabout inhibits N-cadherin-mediated cell adhesion
Activation of the repulsive receptor Roundabout inhibits N-cadherin-mediated cell adhesion
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DOI：
10.1038/ncb858
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发表时间：
2002-10-01
影响因子：
21.3
通讯作者：
VanBerkum, MFA
中科院分区：
文献类型：
--
作者：
Rhee, J;Mahfooz, NS;VanBerkum, MFA
轴突轨迹的形成需要整合的本地粘合剂相互作用与方向信息的吸引力和排斥的线索。在这里，我们表明，这两种类型的信息是功能集成的跨膜受体回旋（机器人）的激活，其配体，分泌排斥性的指导线索缝，灭活N-钙粘蛋白介导的粘附。N-钙粘蛋白介导的粘附的丧失伴随着β-连环蛋白的酪氨酸磷酸化及其从N-钙粘蛋白复合物中的丧失，伴随着含有Robo、Abelson（Abl）激酶和N-钙粘蛋白的超分子复合物的形成。这种受体复合物的局部形成是一种理想的机制，可以引导生长锥，同时仍然允许在其他方向上粘附和生长。
The formation of axon trajectories requires integration of local adhesive interactions with directional information from attractive and repulsive cues. Here, we show that these two types of information are functionally integrated; activation of the transmembrane receptor Roundabout (Robo) by its ligand, the secreted repulsive guidance cue Slit, inactivates N-cadherin-mediated adhesion. Loss of N-cadherin-mediated adhesion is accompanied by tyrosine phosphorylation of beta-catenin and its loss from the N-cadherin complex, concomitant with the formation of a supramolecular complex containing Robo, Abelson (Abl) kinase and N-cadherin. Local formation of such a receptor complex is an ideal mechanism to steer the growth cone while still allowing adhesion and growth in other directions.