Volume 4 Issue 2
Feb.  2013
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Kun Zhu, Xiaoping Chen, Jianghong Liu, Haihong Ye, Li Zhu, Jane Y. Wu. AMPK interacts with DSCAM and plays an important role in Netrin-1 induced neurite outgrowth[J]. Protein&Cell, 2013, 4(2): 155-161. doi: 10.1007/s13238-012-2126-2
Citation: Kun Zhu, Xiaoping Chen, Jianghong Liu, Haihong Ye, Li Zhu, Jane Y. Wu. AMPK interacts with DSCAM and plays an important role in Netrin-1 induced neurite outgrowth[J]. Protein&Cell, 2013, 4(2): 155-161. doi: 10.1007/s13238-012-2126-2

AMPK interacts with DSCAM and plays an important role in Netrin-1 induced neurite outgrowth

doi: 10.1007/s13238-012-2126-2
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This work was supported by the National Basic Research Program (973 Program) (Nos. 2010CB529603 and 2009CB825402) and the National Natural Science Foundation of China (91132710) and Chinese Academy of Science (CASNN-GWPPS-2008). JYW is supported by NIH (RO1AG033004 and R56NS074763) and ALS Therapy Alliance.

  • Received Date: 2012-12-12
  • Rev Recd Date: 2012-12-16
  • 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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