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轴突生长的机制：我们从细胞黏附分子L1中学到的知识。

The mechanism of axon growth: what we have learned from the cell adhesion molecule L1.

作者信息

Kamiguchi Hiroyuki

机构信息

Laboratory for Neuronal Growth Mechanisms, RIKEN Brain Science Institute (BSI), 2-1 Hirosawa, Wako, Saitama 351-0198, Japan.

出版信息

Mol Neurobiol. 2003 Dec;28(3):219-28. doi: 10.1385/MN:28:3:219.

DOI:10.1385/MN:28:3:219
PMID:14709786
Abstract

Cell adhesion molecules (CAMs) are not just an inert glue that mediates static cell-cell and cell-extracellular matrix (ECM) adhesion; instead, their adhesivity is dynamically controlled to enable a cell to migrate through complex environmental situations. Furthermore, cell migration requires distinct levels of CAM adhesivity in various subcellular regions. Recent studies on L1, a CAM in the immunoglobulin superfamily, demonstrate that cell adhesion can be spatially regulated by the polarized internalization and recycling of CAMs. This article examines the molecular mechanism of axon growth, with a particular focus on the role of L1 trafficking in the polarized adhesion and migration of neuronal growth cones.

摘要

细胞黏附分子（CAMs）并非仅仅是介导静态细胞-细胞及细胞-细胞外基质（ECM）黏附的惰性胶水；相反，它们的黏附性受到动态调控，以使细胞能够在复杂的环境中迁移。此外，细胞迁移在不同亚细胞区域需要不同水平的CAM黏附性。最近对免疫球蛋白超家族中的一种CAM——L1的研究表明，细胞黏附可通过CAM的极化内化和再循环在空间上进行调节。本文探讨轴突生长的分子机制，特别关注L1转运在神经元生长锥的极化黏附和迁移中的作用。

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本文引用的文献

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The L1 cell adhesion molecule is essential for topographic mapping of retinal axons.L1细胞黏附分子对于视网膜轴突的拓扑映射至关重要。
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Migration of nerve growth cones requires detergent-resistant membranes in a spatially defined and substrate-dependent manner.神经生长锥的迁移以空间限定且依赖底物的方式需要抗去污剂膜。
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Cis and trans interactions of L1 with neuropilin-1 control axonal responses to semaphorin 3A.
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L1与神经纤毛蛋白-1的顺式和反式相互作用控制轴突对信号素3A的反应。
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