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神经损伤诱导蛋白,一种新型黏附分子,由神经损伤诱导产生并促进轴突生长。

Ninjurin, a novel adhesion molecule, is induced by nerve injury and promotes axonal growth.

作者信息

Araki T, Milbrandt J

机构信息

Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

出版信息

Neuron. 1996 Aug;17(2):353-61. doi: 10.1016/s0896-6273(00)80166-x.

Abstract

Peripheral nerve injury results in axonal degeneration and in phenotypic changes of the surrounding Schwann cells, whose presence is critical for nerve regeneration. Using differential screening strategies, we identified a novel protein, termed ninjurin (for nerve injury-induced protein), that is up-regulated after axotomy in neurons and in Schwann cells surrounding the distal nerve segment. Ninjurin is located on the cell surface, is capable of mediating homophilic adhesion, and promotes neurite extension of dorsal root ganglion neurons in vitro. Ninjurin is also expressed in a number of other tissues, predominantly in epithelial cells. These results suggest that ninjurin plays a role in nerve regeneration and in the formation and function of other tissues.

摘要

周围神经损伤会导致轴突退变以及周围施万细胞的表型变化,而施万细胞的存在对神经再生至关重要。通过差异筛选策略,我们鉴定出一种新的蛋白质,称为神经损伤诱导蛋白(ninjurin),它在轴突切断术后在神经元和远端神经节段周围的施万细胞中上调。Ninjurin位于细胞表面,能够介导同种型黏附,并在体外促进背根神经节神经元的神经突延伸。Ninjurin也在许多其他组织中表达,主要在上皮细胞中。这些结果表明,ninjurin在神经再生以及其他组织的形成和功能中发挥作用。

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