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首页> 外文期刊>Neuron >Myelin-associated glycoprotein interacts with the Nogo66 receptor to inhibit neurite outgrowth.
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Myelin-associated glycoprotein interacts with the Nogo66 receptor to inhibit neurite outgrowth.

机译：髓磷脂相关糖蛋白与Nogo66受体相互作用，抑制神经突向外生长。

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摘要

Myelin inhibitors of axonal regeneration, like Nogo and MAG, block regrowth after injury to the adult CNS. While a GPI-linked receptor for Nogo (NgR) has been identified, MAG's receptor is unknown. We show that MAG inhibits regeneration by interaction with NgR. Binding of and inhibition by MAG are lost if neuronal GPI-linked proteins are cleaved. Binding of MAG to NgR-expressing cells is GPI dependent and sialic acid independent. Conversely, NgR binds to MAG-expressing cells. MAG, but not a truncated MAG that binds neurons but does not inhibit regeneration, precipitates NgR from NgR-expressing cells, DRG, and cerebellar neurons. Importantly, NgR antibody, soluble NgR, or dominant-negative NgR each prevent inhibition of neurite outgrowth by MAG. Also, MAG and Nogo66 compete for binding to NgR. These results suggest redundancy in myelin inhibitors and indicate therapies for CNS injuries.
机译：像Nogo和MAG一样，轴突再生的髓磷脂抑制剂可阻止成年中枢神经系统受伤后的再生。虽然已经确定了Nogo的GPI连锁受体（NgR），但MAG的受体尚不清楚。我们表明，MAG通过与NgR相互作用抑制再生。如果神经元GPI连接的蛋白被切割，则MAG的结合和抑制作用将丧失。 MAG与NgR表达细胞的结合是GPI依赖性和唾液酸依赖性的。相反，NgR与表达MAG的细胞结合。 MAG，但不结合神经元但不抑制再生的截短MAG，则从表达NgR的细胞，DRG和小脑神经元中沉淀NgR。重要的是，NgR抗体，可溶性NgR或显性阴性NgR均可以防止MAG抑制神经突向外生长。同样，MAG和Nogo66竞争与NgR的结合。这些结果表明髓磷脂抑制剂的冗余，并指示中枢神经系统损伤的治疗方法。

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