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体内视网膜神经节细胞轴突生长需要钙黏蛋白发挥功能。

Cadherin function is required for axon outgrowth in retinal ganglion cells in vivo.

作者信息

Riehl R, Johnson K, Bradley R, Grunwald G B, Cornel E, Lilienbaum A, Holt C E

机构信息

Department of Biology, University of California at San Diego, La Jolla 92037-0366, USA.

出版信息

Neuron. 1996 Nov;17(5):837-48. doi: 10.1016/s0896-6273(00)80216-0.

Abstract

The cell-cell adhesion molecule N-cadherin strongly promotes neurite outgrowth in cultured retinal neurons. To test whether cadherins regulate process outgrowth in retinal neurons in vivo, we have blocked cadherin function in single cells by expression of a dominant negative N-cadherin mutant. We report that when cadherin function is inhibited, axon and dendrite outgrowth are severely impaired, particularly in retinal ganglion cells. Laminar migration and cell type specification, by contrast, appear unaffected. Further, expression of the catenin-binding domain of N-cadherin, which blocks cadherin-mediated adhesion in early embryos, does not affect axon outgrowth, suggesting that outgrowth and adhesion are mediated by distinct regions of the cytoplasmic domain. These findings indicate that cadherins play an essential role in the initiation and extension of axons from retinal ganglion cells in vivo.

摘要

细胞间粘附分子N-钙粘蛋白强烈促进培养的视网膜神经元的神经突生长。为了测试钙粘蛋白是否在体内调节视网膜神经元的突起生长,我们通过表达显性负性N-钙粘蛋白突变体来阻断单个细胞中的钙粘蛋白功能。我们报告说,当钙粘蛋白功能受到抑制时,轴突和树突的生长会严重受损,尤其是在视网膜神经节细胞中。相比之下,层状迁移和细胞类型特异性似乎未受影响。此外,N-钙粘蛋白的连环蛋白结合结构域的表达可阻断早期胚胎中钙粘蛋白介导的粘附,但不影响轴突生长,这表明生长和粘附是由细胞质结构域的不同区域介导的。这些发现表明,钙粘蛋白在体内视网膜神经节细胞轴突的起始和延伸中起重要作用。

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