| Literature DB >> 25869138 |
Yonghua Liu1, Youhua Wang1, Ying Chen1, Xiaohong Li1, Jiao Yang1, Yang Liu1, Aiguo Shen2.
Abstract
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.Entities:
Keywords: JNK; SCG10; Spy1; axon; axon loss; molecular cell biology; neurite outgrowth; neurodegenerative disease; phosphorylation; protein phosphorylation; protein stability; protein-protein interaction
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Year: 2015 PMID： 25869138 PMCID： PMC4447963 DOI： 10.1074/jbc.M114.611574
Source DB: PubMed Journal: J Biol Chem ISSN： 0021-9258 Impact factor: 5.157