Axonal Degeneration Is Blocked by Nicotinamide Mononucleotide Adenylyltransferase (Nmnat) Protein Transduction into Transected Axons
Axonal Degeneration Is Blocked by Nicotinamide Mononucleotide Adenylyltransferase (Nmnat) Protein Transduction into Transected Axons
复制标题
DOI：
10.1074/jbc.c110.193904
复制
发表时间：
2010-12-31
影响因子：
4.8
通讯作者：
Milbrandt, Jeffrey
中科院分区：
文献类型：
--
作者：
Sasaki, Yo;Milbrandt, Jeffrey
轴突变性是许多神经系统疾病的早期和重要组成部分。烟酰胺单核苷酸腺苷酰转移酶（Nmnat）是缓慢沃勒变性（Wld（s））蛋白的一种组分，其过表达可保护轴突免受各种损伤。我们发现，Nmnat蛋白转导到切断轴突通过病毒样颗粒防止轴突变性。Nmnat的损伤后功效表明其保护作用局部发生在轴突内，并提供了开发治疗轴突损伤的新型药物的机会。
Axonal degeneration is an early and important component of many neurological disorders. Overexpression of nicotinamide mononucleotide adenylyltransferase (Nmnat), a component of the slow Wallerian degeneration (Wld(s)) protein, protects axons from a variety of insults. We found that transduction of Nmnat protein into severed axons via virus-like particles prevented axonal degeneration. The post-injury efficacy of Nmnat indicates that its protective effects occur locally within the axon and provides an opportunity to develop novel agents to treat axonal damage.