同嗜性神经细胞黏附分子（NCAM）相互作用会干扰L1刺激的神经突生长。

Homophilic NCAM interactions interfere with L1 stimulated neurite outgrowth.

作者信息

Kristiansen L V, Marques F A, Soroka V, Ronn L C, Kiselyov V, Pedersen N, Berezin V, Bock E

机构信息

Protein Laboratory, Institute of Molecular Pathology, University of Copenhagen, Panum Institute, Blegdamsvej 3C, Bld. 6.2, DK-2200, Copenhagen N, Denmark.

出版信息

FEBS Lett. 1999 Dec 24;464(1-2):30-4. doi: 10.1016/s0014-5793(99)01671-3.

DOI:10.1016/s0014-5793(99)01671-3

PMID:10611478

Abstract

The cell adhesion molecules NCAM and L1 are considered to play key roles in neuronal development and plasticity. L1 has been shown to interact with NCAM, possibly through NCAM binding to oligomannosidic glycans present in L1. We investigated the effect of recombinant immunoglobulin (Ig) modules of NCAM involved in homophilic NCAM binding, on L1 induced neurite outgrowth from PC12-E2 cells and found a complete inhibition of L1 induced neurite outgrowth after addition of Ig-modules 1, 2 and 3 of NCAM, suggesting that the ligation state of NCAM is crucial for normal L1 signaling.

摘要

细胞黏附分子NCAM和L1被认为在神经元发育和可塑性中起关键作用。已表明L1可与NCAM相互作用，可能是通过NCAM与L1中存在的寡甘露糖聚糖结合。我们研究了参与NCAM同源结合的重组免疫球蛋白（Ig）模块对L1诱导PC12-E2细胞神经突生长的影响，发现在添加NCAM的Ig模块1、2和3后，L1诱导的神经突生长完全受到抑制，这表明NCAM的连接状态对于正常的L1信号传导至关重要。