Spy1蛋白在轴突退变中介导SCG10蛋白的磷酸化和降解。
Spy1 Protein Mediates Phosphorylation and Degradation of SCG10 Protein in Axonal Degeneration.
作者信息
Liu Yonghua, Wang Youhua, Chen Ying, Li Xiaohong, Yang Jiao, Liu Yang, Shen Aiguo
机构信息
From the Medical College, Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target.
From the Medical College, Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Jiangsu Province Key Laboratory of Neuroregeneration, and Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, China
出版信息
J Biol Chem. 2015 May 29;290(22):13888-94. doi: 10.1074/jbc.M114.611574. Epub 2015 Apr 13.
Axon loss is a destructive consequence of a wide range of neurological diseases without a clearly defined mechanism. Recent data demonstrate that SCG10 is a novel axonal maintenance factor and that rapid SCG10 loss after injury requires JNK activity; how JNK induces degradation of SCG10 is not well known. Here we showed that SCG10 was a binding partner of Spy1, a Speedy/RINGO family protein, which participated in cellular response to sciatic nerve injury. During the early stage of axonal injury, Spy1 expression was inversely correlated with SCG10. Spy1 mediated SCG10 phosphorylation and degradation partly in a JNK-dependent manner. Inhibition of Spy1 attenuated SCG10 phosphorylation and delayed injury-induced axonal degeneration. Taken together, these data suggest that Spy1 is an important regulator of SCG10 and can be targeted in future axo-protective therapeutics.
轴突损失是多种神经疾病的破坏性后果，其机制尚未明确界定。最近的数据表明，SCG10是一种新型的轴突维持因子，损伤后SCG10的快速丧失需要JNK活性；JNK如何诱导SCG10降解尚不清楚。在这里，我们表明SCG10是Spy1（一种Speedy/RINGO家族蛋白）的结合伙伴，后者参与了对坐骨神经损伤的细胞反应。在轴突损伤的早期阶段，Spy1的表达与SCG10呈负相关。Spy1部分以JNK依赖的方式介导SCG10的磷酸化和降解。抑制Spy1可减弱SCG10的磷酸化并延迟损伤诱导的轴突变性。综上所述，这些数据表明Spy1是SCG10的重要调节因子，可作为未来轴突保护治疗的靶点。
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