AMPK interacts with DSCAM and plays an important role in netrin-1 induced neurite outgrowth.
AMPK interacts with DSCAM and plays an important role in netrin-1 induced neurite outgrowth.
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DOI：
10.1007/s13238-012-2126-2
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发表时间：
2013-02
期刊：
影响因子：
21.1
通讯作者：
Wu, Jane Y.
中科院分区：
文献类型：
--
作者：
Zhu, Kun;Chen, Xiaoping;Liu, Jianghong;Ye, Haihong;Zhu, Li;Wu, Jane Y.
关键词：
唐氏综合征细胞粘附分子（DSCAM）作为netrin-1受体，在神经发育中介导轴突对netrin-1的吸引反应。然而，netrin-DSCAM的信号转导机制仍不清楚。在这里，我们报告了AMP活化蛋白激酶（AMPK）通过其γ亚基与DSCAM相互作用，但不与DCC（在结直肠癌中缺失）相互作用，DCC是netrin-1的另一种主要受体。Netrin处理培养的皮层神经元导致AMPK磷酸化增加。显性负效应AMPK突变体和AMPK抑制剂均能显著抑制netrin-1诱导的神经突起生长。总之，这些发现表明AMPK与DSCAM相互作用，并在netrin-1诱导的神经突生长中发挥重要作用。我们的研究揭示了一个以前未知的组件，AMPK，netrin-DSCAM信号通路。
Down syndrome cell adhesion molecule (DSCAM) acts as a netrin-1 receptor and mediates attractive response of axons to netrin-1 in neural development. However, the signaling mechanisms of netrin-DSCAM remain unclear. Here we report that AMP-activated protein kinase (AMPK) interacts with DSCAM through its γ subunit, but does not interact with DCC (deleted in colorectal cancer), another major receptor for netrin-1. Netrin-treatment of cultured cortical neurons leads to increased phosphorylation of AMPK. Both AMPK mutant with dominant-negative effect and AMPK inhibitor can significantly suppress netrin-1 induced neurite outgrowth. Together, these findings demonstrate that AMPK interacts with DSCAM and plays an important role in netrin-1 induced neurite outgrowth. Our study uncovers a previously unknown component, AMPK, in netrin-DSCAM signaling pathway.
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影响因子：
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作者：
Hawley SA;Boudeau J;Reid JL;Mustard KJ;Udd L;Mäkelä TP;Alessi DR;Hardie DG
通讯作者：
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影响因子：
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作者：
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DOI：
10.1073/pnas.0610068104
发表时间：
2007-04-24
影响因子：
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作者：
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通讯作者：
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影响因子：
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作者：
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